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immunity

 
Dictionary: im·mu·ni·ty   (ĭ-myū'nĭ-tē) pronunciation
n., pl., -ties.
  1. The quality or condition of being immune.
  2. Immunology. Inherited, acquired, or induced resistance to infection by a specific pathogen.
  3. Law.
    1. Exemption from normal legal duties, penalties, or liabilities, granted to a special group of people: legislative immunity.
    2. Exemption from legal prosecution, often granted a witness in exchange for self-incriminating testimony.

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Sci-Tech Encyclopedia: Immunity
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A state of resistance to an agent, the pathogen, that normally produces an infection. Pathogens include microorganisms such as bacteria and viruses, as well as larger parasites. The immune response that generates immunity is also responsible in some situations for allergies, delayed hypersensitivity states, autoimmune disease, and transplant rejection. See also Allergy; Autoimmunity; Hypersensitivity; Transplantation biology.

Immunity is engendered by the host immune system, reacting in very specific ways to foreign components (such as proteins) of particular parasites or infective agents. It is influenced by many factors, including the environment, inherited genes, and acquired characteristics. Reaction to a pathogen is through a nonadaptive or innate response as well as an adaptive immune response. The innate response is not improved by repeated encounters with the pathogen. An adaptive response is characterized by specificity and memory: if reinfection occurs, the host will mount an enhanced response.

The components of the pathogen that give rise to an immune response, to which antibodies are generated, are called antigens. There are two types of specific responses to an antigen, antibodies and the cellular response. Antibodies help to neutralize the infectious agent by specifically binding it. A series of proteins in the blood (called complement) act in conjunction with antibodies to destroy pathogenic bacteria. In the cellular response, cytotoxic T cells are recruited to kill cells infected with intracellular agents such as viruses. Helper T cells may also be generated, which influence B cells to produce appropriate antibodies. Inflammatory responses and activation of other kinds of cells, such as macrophages, in conjunction with lymphocytes, is another important aspect of the immune response, as in delayed hypersensitivity. This kind of response seems to be common in certain chronic infections. See also Antibody; Antigen; Complement.

Complex immune systems (antibody and specific cellular responses) have been demonstrated in mammals, birds, amphibians, and fish, and are probably restricted to vertebrates.

Natural or innate immunity

There are natural barriers to infection, both physical and physiological, which are known collectively as innate immunity, and include the effects of certain cells (macrophages, neutrophils and natural killer cells) and substances such as serum proteins, cytokines, complement, lectins, and lipid-binding proteins. The skin or mucous membranes of the respiratory tract are obvious barriers and may contain bacteriostatic or bactericidal agents (such as lysozyme and spermine) that delay widespread infection until other defenses can be mobilized.

If organisms manage to enter tissues, they are often recognized by molecules present in serum and by receptors on cells. Bacterial cell walls, for example, contain substances such as lipopolysaccharides that activate the complement pathway or trigger phagocytic cells. Host range is dramatic in its specificity. Animals and plants are generally not susceptible to each other's pathogens. Within each kingdom, infectious agents are usually adapted to affect a restricted range of species. For example, mice are not known to be susceptible to pneumococcal pneumonia under natural conditions. The health of the host and environmental conditions may also make a difference to susceptibility. This is readily apparent in fish that succumb to fungal infections if their environment deteriorates. Genetic factors have an influence on susceptibility. Some of these genes have been identified, in particular the genes of the major histocompatibility complex which are involved in susceptibility to autoimmune diseases as well as some infectious disorders. See also Histocompatibility.

Once parasites gain entry, phagocytic cells attack them. They may engulf and destroy organisms directly, or they may need other factors such as antibody, complement, or lymphokines, secreted by lymphocytes, which enhance the ability of the phagocytes to take up antigenic material. In many cases these cells are responsible for alerting cells involved in active immunity so there is two-way communication between the innate and adaptive responses. See also Phagocytosis.

Adaptive immune response

Adaptive immunity is effected in part by lymphocytes. Lymphocytes are of two types: B cells, which develop in the bone marrow or fetal liver and may mature into antibody-producing plasma cells, and T cells, which develop in the thymus. T cells have a number of functions, which include helping B cells to produce antibody, killing virus-infected cells, regulating the level of immune response, and controlling the activities of other effector cells such as macrophages.

Each lymphocyte carries a different surface receptor that can recognize a particular antigen. The antigen receptor expressed by B cells consists of membrane-bound antibody of the specificity that it will eventually secrete; B cells can recognize unmodified antigen. However, T cells recognize antigen only when parts of it are complexed with a molecule of the major histocompatibility complex. The principle of the adaptive immune response is clonal recognition: each lymphocyte recognizes only one antigenic structure, and only those cells stimulated by antigen respond. Initially, in the primary response, there are few lymphocytes with the appropriate receptor for an antigen, but these cells proliferate. If the antigen is encountered again, there will be a proportionally amplified and more rapid response. Primed lymphocytes either differentiate into immune effector cells or form an expanded pool of memory cells that respond to a secondary challenge with the same antigen.

The acquired or adaptive immune response is characterized by exquisite specificity such that even small pieces of foreign proteins can be recognized. This specificity is achieved by the receptors on T cells and B cells as well as antibodies that are secreted by activated B cells. The genes for the receptors are arranged in multiple small pieces that come together to make novel combinations, by somatic recombination. Each T or B cell makes receptors specific to a single antigen. Those cells with receptors that bind to the foreign protein and not to self tissues are selected out of a large pool of cells. For T cells, this process takes place in the thymus. The extreme diversity of T- and B-cell receptors means that an almost infinite number of antigens can be recognized. It has been calculated that potentially about 3 × 1022 different T-cell receptors are made in an individual. Even if 99% of these are eliminated because they bind to self tissues, 3 × 1020 would still be available.

Inflammation takes place to activate immune mechanisms and to eliminate thoroughly the source of infection. Of prime importance is the complement system, which consists of tens of serum proteins. A variety of cells are activated, including mast cells and macrophages. Inflammation results in local attraction of immune cells, increased blood supply, and increased vascular permeability. See also Cellular immunology.

Autoimmunity

The immune system is primed to react against foreign antigens while avoiding responses to self tissue by immunological tolerance. Although most T cells which might activate against host proteins are deleted in the thymus, these self-reactive cells are not always destroyed. These exceptions to self tolerance are frequently associated with disease, the autoimmune diseases, which are widespread pathological conditions, including Addison's disease, celiac disease, Goodpasture's syndrome, Hashimoto's thyroiditis, juvenile-onset diabetes mellitus, multiple sclerosis, myasthenia gravis, pemphigus vulgaris, rheumatoid arthritis, Sjögren's disease, and systemic lupus erythematosus. In these diseases, antibodies or T cells activate against self components. See also Autoimmunity.

Immunization

Adaptive immunity is characterized by the ability to respond more rapidly and more intensely when encountering a pathogen for a second time, a feature known as immunological memory. This permits successful vaccination and prevents reinfection with pathogens that have been successfully repelled by an adaptive immune response. Mass immunization programs have led to the virtual eradication of several very serious diseases, although not always on a worldwide scale. Living attenuated vaccines against a variety of agents, including poliomyelitis, tuberculosis, yellow fever, and bubonic plague, have been used effectively. Nonliving vaccines are commonly used for prevention of bacterial diseases such as pertussis, typhoid, and cholera as well as some viral diseases such as influenza and bacterial toxins such as diphtheria and tetanus. See also Cancer (medicine); Vaccination.

Passive immunization

Protective levels of antibody are not formed until some time after birth, and to compensate for this there is passive transfer of antibody across the placenta. Alternatively, in some animals antibody is transferred in the first milk (colostrum). Antibody may also be passively transferred artificially, for example, with a concentrated preparation of human serum gamma globulin containing antibodies against hepatitis. Protection is temporary. Horse serum is used for passive protection against snake venom. Serum from the same (homologous) species is tolerated, but heterologous serum is rapidly eliminated and may produce serum sickness. On repeated administration, a sensitized individual may experience anaphylactic shock, which in some cases is fatal. Cellular immunity can also be transferred, particularly in experimental animal situations when graft and host reactions to foreign tissue invariably occur unless strain tissue types are identical.


Antonyms: immunity
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n

Definition: privilege, exemption
Antonyms: defenselessness, responsibility, susceptibility, vulnerability



In law, exemption or freedom from liability. Under international treaty, a diplomatic representative is exempt from local laws, both civil and criminal. In many countries, judges, legislators, and government officials, including the heads of state, enjoy limited or absolute immunity at home to protect them from personal liability for wrongful acts or omissions that arise from the performance of their duties. A public prosecutor may grant immunity from prosecution to a witness who is suspected of criminal activity in return for testimony against other suspected criminals.

For more information on immunity, visit Britannica.com.

 
Columbia Encyclopedia: immunity
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immunity, ability of an organism to resist disease by identifying and destroying foreign substances or organisms. Although all animals have some immune capabilities, little is known about nonmammalian immunity. Mammals are protected by a variety of preventive mechanisms, some of them nonspecific (e.g., barriers, such as the skin), others highly specific (e.g., the response of antibodies).

Nonspecific Defenses

Nonspecific defenses include physical and chemical barriers, the inflammatory response, and interferons. Physical barriers include the intact skin and mucous membranes. These barriers are aided by various antimicrobial chemicals in tissue and fluids. An example of such a substance is lysozyme, an enzyme present in tears that destroys the cell membranes of certain bacteria.

Inflammatory Response

Another line of defense is the inflammatory response, in which white blood cells called monocytes and granulocytes (e.g., basophils and neutrophils) reach an injured area. Basophils release histamine, which results in increased local blood flow and increased permeability of the capillaries and allows phagocytizing cells, such as neutrophils and monocytes (macrophages), into the area. The same response sometimes results in fever. Leakage of the clotting protein fibrinogen and other substances into the injured area results in blockage of tissue by clots, which wall off the injured area to retard the spread of bacteria or their toxins.

Interferons

Interferons are proteins released by a virus-invaded cell that prompt surrounding cells to produce enzymes that interfere with viral replication. They are the reason that, in most instances, infection with one virus precludes infection by a second virus.

Nonsusceptibility

Nonsusceptibility is the inability of certain disease-carrying organisms to grow in a particular host species. Nonsusceptibility may be caused by such conditions as lack of availability of particular growth substances needed by the infecting microorganism or body temperature unsuitable for the invading microorganism. For example, chickens are nonsusceptible to anthrax because the bacteria cannot grow at the body temperature normal for that animal.

The Immune Response

The principal parts of the immune system are the bone marrow, thymus, lymphatic system, tonsils, and spleen. The lymph nodes, tonsils, and spleen act to trap and destroy antigens from the lymph, air, and blood, respectively. Antigens are molecules that the body reacts to by producing antibodies, highly specific proteins also known as immunoglobulins. Antigens include bacteria and their toxins, viruses, malignant cells, foreign tissues, and the like. Their destruction is accomplished by white blood cells (lymphocytes and the granulocytes and monocytes mentioned above), which are produced and constantly replenished by the stem cells of the bone marrow. The two types of lymphocytes are called B lymphocytes (B cells) and T lymphocytes (T cells). B cells are responsible for production of antibodies in what is called "humoral" immunity after the ancient medical concept of the body humors.

B Lymphocytes

The presence of antigens in contact with receptor sites on the surface of a B lymphocyte stimulates the lymphocyte to divide and become a clone (a line of descendant cells), with each cell of the clone specific for the same antigen. Some cells of the clone, called plasma cells, secrete large quantities of antibody; others, called memory cells, enter a resting state, remaining prepared to respond to any later invasions by the same antigen. Antibody secretion by lymphocytes can be stimulated or suppressed by such variables as the concentration of antigens, the way the antigen fits the lymphocyte's receptor regions, the age of the lymphocyte, and the effect of other lymphocytes.

According to the modified clonal selection theory originally postulated by the Australian immunologist Sir Macfarlane Burnet (for which he was awarded the 1960 Nobel Prize for Physiology or Medicine), a lymphocyte is potentially able to secrete one particular, specific humoral, or free-circulating, antibody molecule. It is believed that early in life lymphocytes are formed to recognize thousands of different antigens, including a group of autoimmune lymphocytes, i.e., cells recognizing antigens of the organism's own body. The immune system is self-tolerant; i.e., it does not normally attack molecules and cells of the organism's own body, because those lymphocytes that are autoimmune are inactivated or destroyed early in life, and the cells that remain, the majority, recognize only foreign antigens. Burnet's theory was confirmed with the development of monoclonal antibodies.

Antibodies

The antibodies produced by B cells are a type of globulin protein called immunoglobulins. There are five classes of immunoglobulins designated IgA, IgD, IgE, IgG, and IgM; gamma globulin (IgG) predominates. Antibody molecules are able to chemically recognize surface portions, or epitopes, of large molecules that act as antigens, such as nucleic acids, proteins, and polysaccharides. About 10 amino acid subunits of a protein may compose a single epitope recognizable to a specific antibody. The fit of an epitope to a specific antibody is analogous to the way a key fits a specific lock. The amino acid sequence and configuration of an antibody were determined in the 1960s by the biochemists Gerald Edelman, an American, and R. R. Porter, an Englishman; for this achievement they shared the 1972 Nobel Prize for Physiology or Medicine.

The antibody molecule consists of four polypeptide chains, two identical heavy (i.e., long) chains and two identical light (i.e., short) chains. All antibody molecules are alike except for certain small segments that, varying in amino acid sequence, account for the specificity of the molecules for particular antigens. In order to recognize and neutralize a specific antigen, the body produces millions of antibodies, each differing slightly in the amino acid sequence of the variable regions; some of these molecules will chemically fit the invading antigen.

Antibodies act in several ways. For example, they combine with some antigens, such as bacterial toxins, and neutralize their effect; they remove other substances from circulation in body fluids; and they bind certain bacteria or foreign cells together, a process known as agglutination. Antibodies attached to antigens on the surfaces of invading cells activate a group of at least 11 blood serum proteins called complement, which cause the breakdown of the invading cells in a complex series of enzymatic reactions. Complement proteins are believed to cause swelling and eventual rupture of cells by making holes in the lipid portion of the cell's membrane.

T Lymphocytes

After their production in the bone marrow, some lymphocytes (called T lymphocytes or T cells) travel to the thymus, where they differentiate and mature. The T cells interact with the body's own cells, regulating the immune response and acting against foreign cells that are not susceptible to antibodies in what is termed "cell-mediated immunity." Three classes of T lymphocytes have been identified: helper T cells, suppressor T cells, and cytotoxic T cells. Each T cell has certain membrane glycoproteins on its surface that determine the cell's function and its specificity for antigens.

One type of function-determining membrane glycoprotein exists in two forms called T4 or T8 (CD4 or CD8 in another system of nomenclature); T4 molecules are on helper T cells, T8 molecules are on suppressor and cytotoxic T cells. Another type of membrane glycoprotein is the receptor that helps the T cell recognize the body's own cells and any foreign antigens on those cells. These receptors are associated with another group of proteins, T3 (CD3), whose function is not clearly understood. T cells distinguish self from nonself with the help of antigens naturally occurring on the surface of the body's cells. These antigens are, in part, coded by a group of genes called the major histocompatibility complex (MCH). Each person's MCH is as individual as a fingerprint.

When a cytotoxic T lymphocyte recognizes foreign antigens on the surface of a cell, it again differentiates, this time into active cells that attack the infected cells directly or into memory cells that continue to circulate. The active cytotoxic T cells can also release chemicals called lymphokines that draw macrophages. Some (the "killer T cells") release cell-killing toxins of their own; some release interferon. Helper T cells bind to active macrophages and B lymphocytes and produce proteins called interleukins, which stimulate production of B cells and cytotoxic T cells. Although poorly understood, suppressor T cells appear to help dampen the activity of the immune system when an infection has been controlled.

Active and Passive Immunity

Naturally acquired active immunity occurs when the person is exposed to a live pathogen, develops the disease, and becomes immune as a result of the primary immune response. Artificially acquired active immunity can be induced by a vaccine, a substance that contains the antigen. A vaccine stimulates a primary response against the antigen without causing symptoms of the disease (see vaccination).

Artificially acquired passive immunity is a short-term immunization by the injection of antibodies, such as gamma globulin, that are not produced by the recipient's cells. Naturally acquired passive immunity occurs during pregnancy, in which certain antibodies are passed from the maternal into the fetal bloodstream. Immunologic tolerance for foreign antigens can be induced experimentally by creating conditions of high-zone tolerance, i.e., by injecting large amounts of a foreign antigen into the host organism, or low-zone tolerance, i.e., injecting small amounts of foreign antigen over long periods of time.

Undesirable Immune Responses and Conditions

Immunity has taken on increased medical importance since the mid-20th cent. For instance, the ability of the body to reject foreign matter is the main obstacle to the successful transplantation of certain tissues and organs. In blood transfusions the immune response is the cause of severe cell agglutination or rupture (lysis) when the blood donor and recipient are not matched for immunological compatibility (see blood groups). An immune reaction can also occur between a mother and baby (see Rh factor). Allergy, anaphylaxis, and serum sickness are all manifestations of undesirable immune responses.

Many degenerative disorders of aging, e.g., arthritis, are thought to be disorders of the immune system. In autoimmune diseases, such as rheumatoid arthritis and lupus, individuals produce antibodies against their own proteins and cell components. Combinations of foreign proteins and their antibodies, called immune complexes, circulating through the body may cause glomerulonephritis (see nephritis) and Bright's disease (a kidney disease). Circulating immune complexes following infection by the hepatitis virus may cause arthritis.

At an extreme end of the spectrum of undesirable conditions is the lack of immunity itself. As a childhood condition, this absence can result from a congenital inability to produce antibodies or from severe disorders of the immune system, which leave individuals unprotected from disease. Such children usually die before adulthood. AIDS (Acquired Immune Deficiency Syndrome), which ultimately destroys the immune system, is caused by a retrovirus called the human immunodeficiency virus (HIV), which was identified in 1981. It infects the helper T cells, thereby disabling the immune system and leaving the person subject to a vast number of progressive complications and death.

Bibliography

See I. Cohen et al., ed., Auto-Immunity (1986); S. Sell, Immunology, Immunopathology, and Immunity (1987); R. Langman, The Immune System (1989); E. Sercarz, ed., Antigenic Determinants and Immune Regulation (1989); J. Kreier, Infection, Resistence, and Immunity (1990)


Law Encyclopedia: Immunity
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This entry contains information applicable to United States law only.

Exemption from performing duties that the law generally requires other citizens to perform, or from a penalty or burden that the law generally places on other citizens.

Sovereign Immunity

Sovereign immunity prevents a sovereign state or person from being subjected to suit without its consent.

The doctrine of sovereign immunity stands for the principle that a nation is immune from suit in the courts of another country, and was first recognized by U.S. courts in the case of The Schooner Exchange v. M'Faddon, 11 U.S. (7 Cranch) 116, 3 L. Ed. 287 (1812). Courts at first espoused a theory providing absolute immunity from the jurisdiction of a U.S. court for any act by a foreign state. But beginning in the early 1900s, courts relied on the political branches of government to define the breadth and limits of sovereign immunity.

In 1952, the U.S. State Department reacted to an increasing number of commercial transactions between the United States and foreign nations by recognizing foreign immunity only in noncommercial or public acts, and not in commercial or private acts. However, the State Department was easily influenced by foreign diplomats requesting absolute sovereign immunity, and the application of sovereign immunity became inconsistent, uncertain, and often unfair.

Complaints about inconsistencies led to the passage of the Foreign Sovereign Immunities Act of 1976 (28 U.S.C.A. §§ 1 note, 1330, 1332, 1391, 1441, 1602-1611). By this act, Congress codified the theory of sovereign immunity, listing exceptions for certain types of acts such as commercial acts, and granted the exclusive power to decide sovereign immunity issues to the courts, rather than the State Department.

Native American tribes have been granted sovereign immunity status by the United States, and therefore generally cannot be sued without the consent of either Congress or the tribe. This immunity is justified by two considerations: First, historically, with more limited resources and tax bases than other governments, Indian tribes have generally been more vulnerable to lawsuits than are other governments. Second, granting sovereign nation status to tribes is in keeping with the federal policy of self-determination for Native Americans.

Indian tribes are immune from suit whether they are acting in a governmental or a proprietary capacity, and immunity is not limited to acts conducted within a reservation. However, individual members of a tribe do not receive immunity for their acts; only the tribe itself is immune as a sovereign nation.

Governmental Tort Immunity

Sovereign immunity may also apply to federal, state, and local governments within the United States, protecting these governments from being sued without their consent. The idea behind domestic sovereign immunity — also called governmental tort immunity — is to prevent money judgments against the government, since such judgments would have to be paid with taxpayers' dollars. As an example, a private citizen injured by another private citizen who runs a red light generally may sue the other driver for negligence. But under a strict sovereign immunity doctrine, a private citizen injured by a city employee driving a city bus has no cause of action against the city unless the city, by ordinance, specifically allows such a suit.

Governmental tort immunity is codified at the federal level by the Federal Tort Claims Act (28 U.S.C.A. § 1291 [1946]), and most states and local governments have similar statutes. Courts and legislatures in many states have greatly restricted, and in some cases abolished, the doctrine of governmental tort immunity.

Official Immunity

The doctrine of sovereign immunity has its roots in the law of feudal England and is based on the tenet that the ruler can do no wrong. Public policy grounds for granting immunity from civil lawsuits to judges and officials in the executive branch of government survive even today. Sometimes known as official immunity, the doctrine was first supported by the U.S. Supreme Court in the 1871 case Bradley v. Fisher, 80 U.S. 335, 20 L. Ed. 646. In Bradley, an attorney attempted to sue a judge because the judge had disbarred him. The Supreme Court held that the judge was absolutely immune from the civil suit because the suit arose from his judicial acts. The Court recognized the need to protect judicial independence and noted that malicious or improper actions by a judge could be remedied by impeachment rather than litigation.

The Court expanded the doctrine to include officers of the federal executive branch twenty-five years later in Spalding v. Vilas, 161 U.S. 483, 16 S. Ct. 631, 40 L. Ed. 780 (1896). In Spalding, an attorney brought a defamation suit against the U.S. postmaster general, who had circulated a letter that criticized the attorney's motives in representing local postmasters in a salary dispute. At that time the postmaster general was a member of the president's cabinet. The Court determined that the proper administration of public affairs by the executive branch of government would be seriously crippled by a threat of civil liability and granted the postmaster general absolute immunity from civil suit for discretionary acts within the scope of the postmaster's authority. Federal courts since Spalding have continued to grant absolute immunity — a complete bar to lawsuits regardless of the official's motive in acting — to federal executive officials, so long as their actions are discretionary and within the scope of their official duties.

In some cases, courts have granted only qualified, rather than absolute, immunity to executive officials. This occurs most often when a statute provides a cause of action for a violation of civil rights by a member of the executive branch of government — for example, when students of a state-run college seek damages from the governor for a violation of their civil rights pursuant to the Civil Rights Act of 1964 (42 U.S.C.A. § 1983). To get qualified immunity, officials must show that they acted without malice and that they reasonably believed that their conduct was legal. Courts employ a two-step analysis to make this determination: first, they analyze whether the statutory or constitutional right asserted by the plaintiff was clear when the wrongful act occurred; second, they decide whether the official should reasonably have known that the action was illegal. An affirmative answer to either of these questions generally results in a denial of immunity to the accused executive official.

In the 1982 case Nixon v. Fitzgerald, 457 U.S. 731, 102 S. Ct. 2690, 73 L. Ed. 2d 349, the Supreme Court held that former U.S. president Richard M. Nixon was entitled to absolute immunity from liability predicated on his official acts as president. In Nixon, a weapons analyst, A. Ernest Fitzgerald, had been fired by the U.S. Air Force after he disclosed to Congress certain cost overruns within the Defense Department. Fitzgerald sued Nixon and two former presidential aides for wrongful retaliatory termination.

The Supreme Court emphasized the singular importance of the duties of the president, and noted that the diversion of the president's energies over concern for private lawsuits "would raise unique risks to the effective functioning of government." The Court also observed that the president, in view of the visibility of the office, would be an easy target for civil lawsuits. A president distracted by this personal vulnerability would prove harmful to the nation.

Immunity from Prosecution

State and federal statutes may grant witnesses immunity from prosecution for the use of their testimony in court or before a grand jury. Sometimes, the testimony of one witness is so valuable to the goals of crime prevention and justice that the promise of allowing that witness to go unpunished is a fair trade. For example, the testimony of a drug dealer that could help law enforcers destroy an entire illegal drug manufacturing network is more beneficial to society than is the prosecution of that lone drug dealer. Although the Fifth Amendment to the U.S. Constitution grants witnesses a privilege against self-incrimination, the U.S. Supreme Court has permitted prosecutors to overcome this privilege by granting witnesses immunity. Prosecutors have the sole discretion to grant immunity to witnesses who appear before a grand jury or at trial.

States employ one of two approaches to prosecutorial immunity: Use immunity prohibits only the witness's compelled testimony, and evidence stemming from that testimony, from being used to prosecute the witness. The witness may still be prosecuted so long as the prosecutor can obtain other physical, testimonial, or circumstantial evidence apart from the witness's testimony. Transactional immunity completely immunizes the witness from prosecution for any offense to which the testimony relates.

Congressional committees have the power to grant testimonial immunity to witnesses who testify before members of Congress. Congressional investigations into allegations of misconduct — such as the Watergate investigations in the 1970s and the Iran-Contra investigations in the 1980s — rely heavily on witness testimony. Whereas prosecutors simply decide whether to grant immunity to a witness, congressional committees must follow more formal procedures. Immunity may be granted only after a two-thirds majority vote by members of the committee, and ten days before the immunized testimony, the committee must advise the Department of Justice or the independent counsel of its intention to grant immunity.

Family Immunity

At common law, a child could sue a parent for breach of contract and for torts related to property. An adult could sue her or his parent for any tort, whether personal or related to property. In 1891, the Mississippi Supreme Court, in Hewllette v. George, 9 So. 885 (1891), held that a child could not seek compensation for personal injury caused by a parent's wrongdoing, so long as the parent and child were obligated by their family duties to one another. The decision was based not on precedent but rather on public policy: the court found that such a lawsuit would undermine the "peace of society and of the families composing society." Criminal laws, the court found, were adequate to protect children.

Other states fell in step with Mississippi, adopting parental immunity of varying degrees. Some parental immunity laws prohibited only claims of negligence, whereas others prohibited lawsuits for intentional torts such as rapes and beatings. The rationale supporting parental immunity laws includes the need to preserve family harmony and, with the availability of liability insurance, the need to prevent parents and the children from colluding to defraud insurance companies.

Unjust results have led courts in many states that espouse parental immunity to carve out exceptions to the rule. For example, a child can usually sue a parent for negligence when the parent has failed to provide food or medical care, but not when the parent has merely exercised parental authority. Most courts have abolished the parental immunity defense for car accident claims, and many allow children to sue their parents for negligent business or employment actions. Courts normally permit wrongful death suits to be brought by a child against a parent or by a parent against a child, because death terminates the parent-child relationship. And most states allow a child to sue a parent for injuries suffered in utero owing to the negligence of the mother.

See: Ambassadors and Consuls; Diplomatic Immunity; Feres Doctrine; Husband and Wife; Judicial Immunity.

Health Dictionary: immunity
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The ability of the body to resist or fight off infection and disease.

Veterinary Dictionary: immunity
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1. the condition of being immune; security against a particular disease; nonsusceptibility to the invasive or pathogenic effects of microorganisms or helminth parasites or to the toxic effect of antigenic substances. Called also functional or protective immunity.
2. responsiveness to antigen that leads to more rapid binding or elimination of antigen than in the nonimmune state; it includes both humoral and cell-mediated immunity (below).
3. the capacity to distinguish foreign material from self, and to neutralize, eliminate or metabolize that which is foreign (non-self) by the physiological mechanisms of the immune response.
The mechanisms of immunity are essentially concerned with the body's ability to recognize and dispose of substances which it interprets as foreign and sometimes harmful to its well-being. When such a substance enters the body, complex chemical and mechanical activities are set into motion to defend and protect the body's cells and tissues. The foreign substance, usually a protein, is called an antigen, that is, one which generates the production of an antagonist. The most readily recognized response to the antigen is the production of antibody. The antigen–antibody reaction is an essential component of the overall immune response. Of equal or greater importance to antibody, particularly for some antigens, is the development of so-called cell-mediated immune response, which involves clonal expansion of specifically reactive T lymphocytes including cytotoxic T lymphocytes (Tc lymphocytes) which play a major role in eliminating the foreign antigens that are cell associated.
Immunological responses in animals can be divided into two broad categories: humoral immunity, which refers to the production of antibody which becomes part of the body fluids (humors), especially serum, and cell-mediated or cellular immunity, which involves a variety of activities designed to destroy or at least contain cells that are recognized by the body as expressing foreign antigens on their cell surface, e.g. viral antigens. Both types of response are mediated by lymphocytes that originate in the bone marrow as stem cells and later are converted into mature cells having specific properties and functions.

  • acquired i. — antigen specific immunity attributable to the production of antibody and of specific immune T lymphocytes (responsible for cell-mediated immunity), following exposure to an antigen, or passive transfer of antibody or immune lymphoid cells (adoptive immunity).
  • active i. — that which follows exposure to an antigen; acquired immunity attributable to the presence of antibody or of immune lymphoid cells formed in response to antigenic stimulus. Called also adaptive immunity.
  • adoptive i. — passive immunity of the cell-mediated type conferred by the administration of sensitized lymphocytes from an immune donor to a naive recipient.
  • artificial i. — includes acquired (active) immunity produced by deliberate exposure to an antigen, such as a vaccine or the administration of antibody (passive).
  • cellular i. — dependent upon T lymphocytes which are sensitized by first exposure to a specific antigen. Subsequent exposure stimulates the release of a group of substances known as lymphokines, such as interferon, and interleukins as well as direct killing by cytotoxic T lymphocytes.
  • functional i. — see immunity (above).
  • humoral i. — mediated by antibodies formed by antigen-specific B lymphocytes. Each B lymphocyte has monomeric IgM receptors which capture specific antigen, initiating production of the specific immunoglobulins. B lymphocytes activated by the presence of their specific antigen undergo transformation, lymphocyte blastogenesis, whereby they become metabolically active, divide, and some mature to plasma cells, which are major producers of antibodies. Some cells revert to small lymphocytes, ‘memory’ cells, and the expanded clone of these cells, on re-exposure to the antigen, undergo further lymphocyte blastogenesis, leading to further increased antibody production and numbers of memory cells.
  • — There are two types of humoral immune response: primary and secondary. The primary response begins immediately after the inital contact with an antigen; the resulting antibody, predominantly IgM, appears 48 to 72 hours later. The secondary response occurs within 24 to 48 hours and produces large quantities of predominantly IgG. The secondary response persists much longer than the primary response and is the result of repeated contact with the antigens.
  • innate i., native i., natural i. — natural immunity resulting from the genetic makeup of the host, before exposure to an antigen.
  • maternal i. — that acquired by the neonate by transplacental transfer of immunoglobulins or from ingestion of colostrum or via the yolk sac in the case of birds. The placentation of all agricultural animals precludes trans-placental transfer of immunoglobulin. Passive transfer of maternal immunity is effected by the transfer of immunoglobulilns present in high concentration in the first milk, colostrum, through the intestine of the newborn. The success of this transfer is dependent upon the time after birth that colostrum is ingested (physiologically 24–36 hours, but effectively for adequate transfer, 8 hours after birth) and on the mass of immunoglobulin ingested which is determined by the concentration of immunoglobulin in colostrum and the amount of colostrum ingested.
  • Failure of passive transfer results in a significant increase in risk for neonatal disease. Neonates that fail to acquire serum concentrations of IgG1 greater than 10 mg/ml are at significantly higher risk of septicemic, enteric and respiratory disease. Failure of passive transfer occurs as a result of neonates sucking the dam or acquiring colostrum by artificial feeding too late in the absorptive process, or by receiving too little colostrum or receiving colostrum with low immunoglobulin concentration. See also passive immunity (below) and colostral immunoglobulin.
  • natural i. — see innate immunity (above).
  • passive i. — the transfer of antibodies from a donor in which they were produced to a recipient for temporary immunity. Can be in the form of serum or colostrum or yolk. Significant transplacental transfer of antibodies is found in primates, but does not occur in domestic animals. Passive immunity in domestic mammals comes via the colostrum, with its high concentration of antibodies, and the more than normally pervious epithelium of the neonate's intestinal epithelium. In birds maternal antibody is transferred to the yolk, from where the developing chick embryo absorbs it from about day 11 of incubation. See also passive immunization.
  • protective i. — see immunity (above).
Wikipedia: Immunity
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Immunity may refer to:

Medicine

  • Immunity (medical), resistance of an organism to infection or disease
  • Immunity (journal), an academic medical journal that publishes research on the immune system.

Law

Other


Translations: Immunity
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Dansk (Danish)
n. - immunitet, uimodtagelighed, ukrænkelighed

Nederlands (Dutch)
onschendbaarheid

Français (French)
n. - (Méd, Admin) immunité, impassibilité, exemption

Deutsch (German)
n. - Immunität, Unempfänglichkeit, Freiheit

Ελληνική (Greek)
n. - απαλλαγή, εξαίρεση, ασυλία, ασυδοσία, ατιμωρησία, (ιατρ.) ανοσία

Italiano (Italian)
immunità

Português (Portuguese)
n. - imunidade (f)

Русский (Russian)
иммунитет, неприкосновенность, освобождение, льгота

Español (Spanish)
n. - inmunidad, exención

Svenska (Swedish)
n. - immunitet, frihet

中文(简体)(Chinese (Simplified))
免疫, 免除, 免疫性

中文(繁體)(Chinese (Traditional))
n. - 免疫, 免除, 免疫性

한국어 (Korean)
n. - 면제, 면역

日本語 (Japanese)
n. - 免疫, 免疫性, 免除

العربيه (Arabic)
‏(الاسم) حصانه, مناعه‏

עברית (Hebrew)
n. - ‮חסינות, פטור, שחרור‬


 
 

 

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