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Untitled - D Ank Unlimited

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EAE 240 Echinococcus immunity<br />

and complement, encircle human B lymphocytes to form a<br />

rosette. This is based on erythrocyte binding to C3b receptors.<br />

This technique has been used in the past to identify B<br />

lymphocytes. However, phagocytic cells bearing C3b receptors<br />

may also form EAC rosettes. This type of rosette is in<br />

contrast to the E rosette that identifies T lymphocytes. B<br />

lymphocytes are now enumerated by monoclonal antibodies<br />

against the B lymphocyte CD (cluster of differentiation)<br />

markers using flow cytometry.<br />

EAE<br />

Acronym for experimental allergic encephalomyelitis.<br />

EAM<br />

Refer to experimental autoimmune myocarditis.<br />

EAMG<br />

Refer to experimental autoimmune myasthenia gravis.<br />

The condition can be induced in more than one species of<br />

animals by immunizing them with purified AchR from<br />

the electric ray (Torpedo californica). The autoantigen,<br />

nicotinic AchR, is T cell-dependent. The in vivo synthesis<br />

of anti-AchR antibodies requires helper T cell activity.<br />

Antibodies specific for the nicotinic acetylcholine receptors<br />

(AchRs) of skeletal muscle react with the postsynaptic<br />

membrane at the neuromuscular junction.<br />

early B-cell factor (EBF)<br />

A transcription factor requisite for early B cell development<br />

and for RAG expression.<br />

early induced responses<br />

Nonadaptive host responses induced by infectious agents<br />

early in infection. The inductive phase of these responses<br />

differentiates them from innate immunity, and their failure<br />

to involve clonal selection of antigen-specific lymphocytes<br />

distinguishes them from adaptive immunity.<br />

early phase reaction<br />

A Type I hypersensitivity elicitation response characterized<br />

by the rapid development of clinical symptoms following<br />

the release of preformed inflammatory mediators from mast<br />

cells undergoing degranulation.<br />

early pro-B cell<br />

Refer to pro-B cell.<br />

early signalosome<br />

The initial TCR signal transduction molecular complex<br />

capable of participating in either the immunosome or the<br />

telerosome.<br />

EAT<br />

Abbreviation for experimental autoimmune thyroiditis.<br />

Includes a murine model for Hashimoto’s thyroiditis.<br />

There is a strong major histocompatibility complex (MHC)<br />

genetic component in susceptibility to Hashimoto’s thyroiditis,<br />

which has been shown to reside in the IA subregion<br />

of the murine MHC (H-2), governing the immune response<br />

(Ir) genes to mouse thyroglobulin (MTg). Following induction<br />

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

and mononuclear cells infiltrate the thyroid. Repeated<br />

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

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

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

stimulation with MTg. The disease can be passively<br />

transferred to naïve recipients by adoptive immunization<br />

and differentiate into oxytotoxic T lymphocytes (T c) in<br />

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

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

murine-autoreactive T cells have been found to show a good<br />

correlation with susceptibility to EAT and to be dependent<br />

on 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.<br />

T lymphocytes cloned from thyroid infiltrates of patients<br />

with Hashimoto’s thyroiditis reveal numerous cytotoxic T<br />

lymphocytes and clones synthesizing interleukin-2 (IL2)<br />

and interferon-γ (IFN-γ). While the T cell subsets participate<br />

in pathogenesis of Hashimoto’s thyroiditis, autoantibody<br />

synthesis appears to aid perpetuation of the disease or<br />

result from it.<br />

EAU<br />

Refer to experimental autoimmune uveoretinitis.<br />

EBF (early B cell factor)<br />

A transcription factor requisite for early B cell development<br />

and for recombinase-activating gene (RAG) expression.<br />

EBI1<br />

An orphan chemokine receptor expressed on normal<br />

lymphoid tissues as well as several B and T lymphocyte<br />

cell lines. EBI1 mRNA is detected in Epstein–Barr virus<br />

(EBV)-positive B cell lines. The tissue source is EBVinduced<br />

cDNA. Also termed BLR2.<br />

EBNA (Epstein–Barr virus nuclear antigen)<br />

Refer to Epstein–Barr nuclear antigen.<br />

ECF-A (eosinophil chemotactic factor of anaphylaxis)<br />

A 500-D acidic polypeptide that attracts eosinophils.<br />

Interaction of antigen with immunoglobulin E (IgE) antibody<br />

molecules on the surface of mast cells causes ECF-A<br />

to be released from the mast cells.<br />

E-cadherin (ECH-6), mouse<br />

Anti-E-cadherin mouse monoclonal antibody detects<br />

E-cadherin, an adhesion protein expressed in cells of epithelial<br />

lineage. It stains positively in glandular epithelium and in<br />

adenocarcinomas of the lung, GI tract, and ovary. It has been<br />

useful in distinguishing adenocarcinoma from mesothelioma. It<br />

has also been shown to be positive in some thyroid carcinomas.<br />

Echinococcus immunity<br />

The genus Echinococcus includes four species of tapeworm<br />

parasites, among which is Echinococcus granulosus.<br />

Its cycle of transmission involves interaction between a<br />

definitive host, such as a carnivore, and an intermediate<br />

host (herbivore or omnivore). Each host may reveal two<br />

morphologically distinct parasite stages. Definitive hosts<br />

are infected with the tapeworm stage of Echinococcus.<br />

Immunological methods have been used to diagnose infection<br />

in definitive hosts and to develop a recombinant vaccine<br />

that is highly effective in protecting sheep from hydatid<br />

infection. Ovine hydatid cyst fluid is rich in antigen. The<br />

principal parasite antigens are designated antigen 5 and<br />

antigen B. Antibodies against these are useful in immunodiagnosis<br />

of hydatid infection in humans; 27- and 94-kDA<br />

protein antigens from protoscoleces are recognized by sera<br />

of dogs infected with E. granulosus; 22-, 30-, and 37-kDA<br />

oncosphere antigens are specific for E. granulosus and are<br />

stage-specific for oncospheres. Little is known regarding<br />

cellular responses against E. granulosus infection in dogs,<br />

but T cells and activated macrophages are believed to play a<br />

significant role in cellular immunity against Echinococcus<br />

in intermediate hosts. With respect to the humoral immune<br />

response to infection, dogs form immunoglobulin A<br />

(IgA), IgG, and IgM antibodies against E. granulosus.<br />

IgA antibody against E. granulosus is produced in the

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