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Untitled - D Ank Unlimited

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tissue transglutaminase autoantibodies 705 Tla complex<br />

Arne W.K. Tiselius.<br />

expressed inappropriately in a neoplastic cell, it may be<br />

called a tumor-associated antigen.<br />

tissue transglutaminase autoantibodies<br />

Immunoglobulin A (IgA) autoantibodies against tissue<br />

transglutaminase (tTG) that have a close correlation with<br />

active celiac disease. tTG is an intracellular enzyme found<br />

in the endomysium and is released after cellular injury or<br />

wounding. The enzyme facilitates deamidation of extracellular<br />

proteins including gluten peptides, leading to<br />

enhanced T cell stimulatory activity. tTG antibodies are<br />

transient, disappearing when gluten is eliminated from the<br />

diet and mucosal healing occurs. Available data suggest that<br />

tTG autoantibodies are very specific for celiac disease.<br />

tissue typing<br />

The identification of major histocompatibility complex<br />

(MHC) class I and class II antigens on lymphocytes by<br />

serological and cellular techniques. The principal serological<br />

assay is microlymphocytotoxicity using microtiter<br />

plates containing predispensed antibodies against human<br />

leukocyte antigen (HLA) specificities to which lymphocytes<br />

of unknown specificity plus rabbit complement and vital<br />

dye are added. Following incubation, the wells are scored<br />

according to the relative proportion of cells killed. This<br />

method is employed for organ transplants such as renal<br />

allotransplants. For bone marrow transplants, the earlier<br />

mixed lymphocyte culture (MLC, also called mixed lymphocyte<br />

reaction) procedure was performed to determine<br />

the relative degree of histocompatibility or histoincompatibility<br />

between donor and recipient. The older cellular<br />

and serological techniques have been replaced largely by<br />

molecular (DNA) typing procedures employing polymerase<br />

chain reaction (PCR) methodology and DNA or oligonucleotide<br />

probes, especially for MHC class II typing. Sequencespecific<br />

primer (SSP) technology is the current choice for<br />

molecular typing. In addition to PCR-based probe hybridization<br />

techniques, restriction fragment length polymorphisms<br />

and direct amplicon analysis methods are also<br />

employed. Panel-reactive antibody analysis by Luminexx ®<br />

or an equivalent instrument is useful also for antibody identification<br />

in post-transplant monitoring.<br />

titer<br />

An approximation of the antibody activity in each unit<br />

volume of a serum sample. The term is used in serology.<br />

Titer is determined by preparing serial dilutions of antibody<br />

to which a constant amount of antigen is added. The end<br />

point is the highest dilution of antiserum in which a visible<br />

reaction with antigen (e.g., agglutination) can be detected.<br />

Titer is expressed as the reciprocal of the serum dilution<br />

that defines the end point. If agglutination occurs in a tube<br />

containing a 1:240 dilution, the antibody titer is said to be<br />

240, that is, the serum contains approximately 240 units<br />

of antibody per milliliter of antiserum. Titer provides only<br />

an estimate of antibody activity. For absolute amounts of<br />

antibody, quantitative precipitation or other methods must<br />

be employed.<br />

TL (thymic leukemia) antigen<br />

An epitope on the thymocyte membranes of TL + mice. As<br />

the T lymphocytes mature, this antigen disappears, but it<br />

resurfaces if leukemia develops. TL antigens are specific<br />

and normally present on surfaces of thymocytes of certain<br />

mouse strains. They are encoded by a group of structural<br />

genes located at the Tla locus, in the linkage group IX,<br />

very near the D pole of the H-2 locus on chromosome 17.<br />

One of the three structural TL genes has two alleles. The<br />

TL antigens are numbered from 1 to 4, specifying four<br />

antigens: TL.1, TL.2, TL.3, and TL.4. TL.3 and TL.4 are<br />

mutually exclusive. Their expression is under the control<br />

of regulatory genes, apparently located at the same Tla<br />

locus. Normal mouse thymocytes belong to three phenotypic<br />

groups: TL, TL.2, and TL.1, 2, 3. Development of<br />

leukemia in mice induces a restructuring of the TL surface<br />

antigens of thymocytes with expression of TL.1 and TL.2 in<br />

TL cells, expression of TL.1 in TL.2 cells, and expression<br />

of TL.4 in both TL and TL.2 cells. When normal thymic<br />

cells leave the thymus, the expression of TL antigen ceases.<br />

Thus, thymocytes are TL (except the TL strains) and the<br />

peripheral T cells are TL. In transplantation experiments,<br />

TL tumor cells undergo antigenic modulation. Tumor cells<br />

exposed to the homologous antibody stop expressing the<br />

antigen and thus escape lysis when subsequently exposed to<br />

the same antibody plus complement.<br />

Tla antigen<br />

Murine major histocompatibility complex (MHC) class I<br />

histocompatibility antigen encoded by genes situated near<br />

the Qa region on chromosome 17. Thymocytes may express<br />

products of up to six alleles. Leukemia cells may aberrantly<br />

express Tla antigens.<br />

Tla complex<br />

Genes that map to the major histocompatibility complex<br />

(MHC) region telomeric to H2 loci on chromosome 17 in<br />

mice. These genes encode MHC class I proteins such as Qa<br />

and Tla that have no known immune function. Qa and Tla<br />

proteins that closely resemble H2 MHC class I proteins in<br />

sequence associate noncovalently with β 2 microglobulin.<br />

Expression of Qa and Tla proteins, unlike expression of<br />

MHC H-2 class I proteins, is limited to only selected mouse<br />

cells. For example, only hepatocytes express Q10 protein,<br />

only selected lymphocyte subpopulations such as activated<br />

T lymphocytes express Qa-2 proteins, and T lymphocytes<br />

express Tla proteins. Thus, Qa and Tla class I molecules<br />

differ in structure and expression from the remaining<br />

MHC class I genes and proteins in mice. This may account<br />

T

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