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experimental autoimmune sialoadenitis (EAS) 258 extrinsic asthma<br />

The infiltrating lymphocytes are comprised mainly of CD4 +<br />

T lymphocytes. There are also many macrophages, and<br />

immunoglobulin G (IgG) is found in the zona pellucida.<br />

experimental autoimmune sialoadenitis (EAS)<br />

An animal model used to investigate the pathogenesis of<br />

salivary gland injury in Sjögren’s syndrome. It may be<br />

induced in LEW rats by immunization with allogeneic or<br />

syngeneic submandibular gland tissue in complete Freund’s<br />

adjuvant and Bordetella pertussis. Autoantibodies are produced<br />

against antigens of salivary ducts as well as mononuclear<br />

cell infiltration of salivary tissues, comprised of<br />

CD4 + , CD8 + , and B lymphocytes. Injury of glands is acute,<br />

yet tissue damage resolves spontaneously 4 to 5 weeks after<br />

immunization. CD4 + T lymphocytes play a critical role in<br />

EAS induction.<br />

experimental autoimmune thyroiditis (EAT)<br />

A murine model for Hashimoto’s thyroiditis. Susceptibility<br />

to Hashimoto’s thyroiditis has a strong major histocompatibility<br />

complex (MHC) genetic component, which has<br />

been shown to reside in the IA subregion of the murine<br />

MHC (H-2), governing the immune response (Ir) genes<br />

to mouse thyroglobulin (MTg). Induced by immunizing<br />

CBA/J mouse substrains with Freund’s complete adjuvant<br />

with whole thyroglobulin protein or its peptides. Following<br />

induction of EAT with MTg, autoantibodies against MTg<br />

appear, and mononuclear cells infiltrate the thyroid.<br />

Repeated administration of soluble, syngeneic MTg without<br />

adjuvant leads to thyroiditis only in the murine haplotype<br />

susceptible to EAT. Autoreactive T cells proliferate in vitro<br />

following stimulation with MTg, passively transfer the<br />

disease to naïve recipients by adoptive immunization and<br />

differentiate into cytotoxic T lymphocytes (T c) in vitro.<br />

Thus, lymphoid cells rather than antibodies represent the<br />

primary mediators of the disease. In vitro proliferation of<br />

murine-autoreactive T cells was found to show a good correlation<br />

with susceptibility to EAT and was dependent on<br />

the presence of Thy-1 + , Lyt-1 + , Ia + , and L3T4 + lymphocytes.<br />

Effector T lymphocytes (T E) in EAT comprise various<br />

T cell subsets and Lyt-1 (L3T4) and Lyt-2 phenotypes. T<br />

lymphocytes cloned from thyroid infiltrates of patients<br />

with Hashimoto’s thyroiditis reveal numerous cytotoxic<br />

T lymphocytes and clones synthesizing IL-2 and IFN-γ.<br />

While the T cell subsets participate in the pathogenesis of<br />

Hashimoto’s thyroiditis, autoantibody synthesis appears to<br />

aid perpetuation of the disease or result from it.<br />

experimental autoimmune uveitis (EAU)<br />

A disease of the neural retina and related tissues induced by<br />

immunization with purified retinal antigens. It is a model<br />

for various human ocular inflammatory diseases, possibly<br />

autoimmune, that are accompanied by immunologic<br />

responses to ocular antigens. The most frequently used are<br />

retinal soluble antigen (S-Ag), the interphotoreceptor retinoid-binding<br />

protein (IRBP), and rhodopsin. Immunization<br />

with these antigens incorporated into complete Freund’s<br />

adjuvant leads to injury of the photoreceptor cell layer of<br />

the retina. Histopathologically, inflammatory cells infiltrate<br />

the retina, and the photoreceptors are injured. Also called<br />

experimental autoimmune uveoretinitis.<br />

experimental tolerance<br />

Antigen-specific suppression of an immune response<br />

induced by the inoculation of a mature animal with a nonimmunogenic<br />

form of the antigen through the usual manner<br />

of immunization or an immunogenic form of the antigen<br />

through a nonimmunogenic route of administration.<br />

extended haplotype<br />

Linked alleles in positive linkage disequilibrium situated<br />

between and including HLA-DR and HLA-B of the major<br />

histocompatibility complex (MHC) of humans. Examples<br />

of extended haplotypes include the association of B8/DR3/<br />

SCO1/GLO2 with membranoproliferative glomerulonephritis<br />

and of A25/B18/DR2 with complement C2 deficiency.<br />

Extended haplotypes may be consequences of crossover<br />

suppression through environmental influences together<br />

with selected HLA types, leading to autoimmune conditions.<br />

The B27 relationship to Klebsiella is an example.<br />

Polymerase chain reaction (PCR) amplification and direct<br />

sequencing help identify a large number of allelic differences<br />

and specific associations of extended haplotypes<br />

with disease. Extended haplotypes are more informative<br />

than single polymorphisms. Some diseases associated with<br />

extended haplotypes include Graves’ disease, pemphigus<br />

vulgaris, type I (juvenile onset) psoriasis, insulin-dependent<br />

diabetes mellitus, celiac disease, and autoimmune hepatitis.<br />

extracellular antigen<br />

Refer to exogenous antigen.<br />

extracellular pathogen<br />

A pathogenic microorganism that reproduces in the interstitial<br />

fluid, blood or lumens of the respiratory, urogenital, and<br />

gastrointestinal tracts rather than entering host cells.<br />

extramedullary plasmacytoma<br />

A plasma cell dyscrasia in which the malignant plasma cells<br />

have moved beyond the bone marrow and entered other tissues.<br />

extramedullary tissues<br />

Tissues and organs other than lymphoid tissues or bone<br />

marrow.<br />

extranodal lymphoma<br />

A lymphoma of diffuse lymphoid tissue, such as gut-associated<br />

lymphoid tissue.<br />

extrathymic T cell development<br />

Development and maturation of T lymphocytes in tissues<br />

external to the thymus gland.<br />

extravasation<br />

The movement of fluid and cells from the circulating<br />

blood into the surrounding tissues without interrupting the<br />

integrity of vessel walls, as in inflammation. The process<br />

consists of margination and diapedesis.<br />

extrinsic allergic alveolitis<br />

Inflammation in the lung produced by immune reactivity,<br />

mainly of the granulomatous type, to inhaled antigens such<br />

as dust, bacteria, molds, grains, and other substances. Also<br />

called farmer’s lung.<br />

extrinsic apoptotic pathway<br />

Refer to apoptosis.<br />

extrinsic asthma<br />

An asthma caused by antigen-antibody reactions. It has<br />

two mutually non-exclusive forms: (1) atopic, involving

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