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Untitled - D Ank Unlimited

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infectious mononucleosis syndromes 388 inflammatory mediator<br />

EBV. Splenomegaly and chemical hepatitis may also be<br />

present.<br />

infectious mononucleosis syndromes<br />

Conditions induced by viruses that produce an acute and<br />

striking peripheral blood monocytosis and lead to symptoms<br />

resembling those of infectious mononucleosis induced by<br />

Epstein–Barr virus. Examples include herpes virus, cytomegalovirus,<br />

HIV-1, HHV-6, and Toxoplasma gondii infections.<br />

infectious tolerance<br />

A state in which induced peripheral tolerance to a given<br />

antigen is transmitted from an anergic T cell population to<br />

a population of normal T cells that are rendered tolerant to<br />

the same antigen. This phenomenon may be mediated by<br />

regulatory T cells. Infectious tolerance was described in the<br />

1970s. Animals rendered tolerant to foreign antigens were<br />

found to possess suppressor T lymphocytes associated with<br />

the induced unresponsiveness. Thus, self tolerance was postulated<br />

to be based on the induction of suppressor T cells.<br />

Noel Rose referred to this concept as clonal balance rather<br />

than clonal deletion. Self antigens are considered to normally<br />

induce mostly suppressor rather than helper T cells,<br />

leading to a negative suppressor balance in the animal body.<br />

Three factors with the potential to suppress immune reactivity<br />

against self include nonantigen-specific suppressor T<br />

cells, antigen-specific suppressor T cells, and anti-idiotypic<br />

antibodies. Rose suggested that suppressor T lymphocytes<br />

leave the thymus slightly before the corresponding helper T<br />

cells. Suppressor T cells specific for self antigens are postulated<br />

to be continuously stimulated and usually in greater<br />

numbers than the corresponding helper T cells.<br />

infertility, immunological<br />

Infertility in 12 to 25% of cases in which infertile couples<br />

are unable to conceive even though they manifest no significant<br />

abnormalities upon physical examination. These cases<br />

of unexplained infertility may be caused by autoimmune<br />

responses to organ-specific antigens of the reproductive<br />

tracts of both males and females and isoimmune reactions<br />

of females against semen components. Immune responses<br />

may cause or contribute to infertility in approximately 10%<br />

of these couples.<br />

inflammation<br />

A defense reaction of living tissue to injury. Plays an<br />

integral role in both innate and adaptive immunity.<br />

Inflammatory cells phagocytize antigen, generate chemical<br />

signals that facilitate wound healing, and secrete<br />

cytokines and chemokines that attract and regulate<br />

lymphocytes. The literal meaning of the word is burning,<br />

and it originates from the cardinal symptoms of rubor,<br />

calor, tumor, and dolor, the Latin terms equivalent to redness,<br />

heat, swelling, and pain, respectively. Inflammation<br />

is beneficial for the host and essential for survival of the<br />

species, although in some cases the response is exaggerated<br />

and may be itself injurious. Inflammation is the<br />

result of multiple interactions that have as a first objective<br />

localization of the process and removal of the irritant.<br />

This is followed by a period of repair. Inflammation<br />

is not necessarily of an immunologic nature, although<br />

immunologic reactions are among the immediate causes<br />

inducing inflammation and the immunologic status of<br />

the host determines the intensity of the inflammatory<br />

response. Inflammation tends to be less intense in infants,<br />

whose immune systems are not fully mature. The causes<br />

of inflammation are numerous and include living microorganisms<br />

such as pathogenic bacteria and animal parasites<br />

that act mainly by the chemical poisons they produce and<br />

less by mechanical irritation; viruses that become offenders<br />

after they multiply in the host and cause cell damage;<br />

and fungi that grow at the surface of the skin but produce<br />

little or no inflammation in the dermis. Other causes of<br />

inflammation include physical agents such as trauma, thermal<br />

and radiant energy, and chemical agents that represent<br />

a large group of exogenous or endogenous causes including<br />

immunologic offenders. Mediators of inflammation<br />

include kinins, acute phase proteins, leukotrienes, prostaglandins,<br />

and vasoactive amines including histamine.<br />

Refer to inflammatory response.<br />

inflammatory bowel disease (IBD)<br />

A general term that applies to ulcerative colitis, Crohn’s<br />

disease, and idiopathic inflammatory bowel disease that<br />

resembles the other two. There is a hereditary predisposition<br />

to IBD. Intestinal epithelial cells express HLA-DR<br />

(MHC class II) antigens in Crohn’s disease, ulcerative<br />

colitis, and infectious colitis patients that may render the<br />

antigens capable of becoming autoantigen-presenting cells.<br />

Inflammatory bowel disease patients may become sensitized<br />

to cow’s milk antigens, developing IgG and IgM antibodies<br />

against this protein. Leukotrienes have been shown<br />

to be of greater significance than prostaglandins in mediating<br />

inflammation in ulcerative colitis. Mucocutaneous<br />

conditions such as oral ulcers, epidermolysis bullosa<br />

acquisita, erythema nodosa, etc., and eye diseases such<br />

as uveitis and iridocyclitis may be associated with IBD.<br />

Some IBD patients may also have cirrhosis, chronic active<br />

hepatitis, or joint involvement such as ankylosing spondylitis.<br />

IBD patients may have abdominal pain, fever, and<br />

diarrhea. Granulomas may develop in the gut wall, and<br />

lymphocytes that stain for IgA in the cytoplasm are often<br />

abundant. Autoantibodies reactive with fetal colon antigens<br />

may be present. IBD develops in gene knockout mice<br />

lacking interleukin-2 (IL2), IL10, or the TCR-α chain.<br />

Inflammation is mediated in part through the action of<br />

cytokines that include IL1α, IL1β, IL6, or tumor necrosis<br />

factor α (TNF-α). IL1α and IL1β induce fever, stimulate<br />

acute phase protein synthesis, and activate the immune system.<br />

TNF-α and IL6 enhance cellular catabolism, induce<br />

acute phase proteins, and stimulate pyrogenic activity.<br />

TNF-α can induce IL1 and IL6. TNF-α and IL2 stimulate<br />

prostaglandin I 2 (PGIL 2), prostaglandin E (PGE 2), and<br />

platelet-activating factor (PAF) secretion.<br />

inflammatory CD4 T cell<br />

Armed effector T H1 cell that synthesizes interferon γ<br />

(IFN-γ) and tumor necrosis factor (TNF) cytokines when it<br />

recognizes antigen. Its principal function is to activate macrophages.<br />

Selected T H1 cells may also mediate cytotoxicity.<br />

inflammatory cells<br />

Cells of the blood and tissues that participate in acute and<br />

chronic inflammatory reactions. They include polymorphonuclear<br />

neutrophils, eosinophils, and macrophages.<br />

inflammatory macrophage<br />

A macrophage in a peritoneal exudate induced by thioglycolate<br />

broth or mineral oil injection into the peritoneal<br />

cavity of an experimental animal.<br />

inflammatory mediator<br />

A substance that participates in an inflammatory reaction.

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