Mouse anti-Rat TCR alpha/beta Monoclonal antibody, clone S84

Although each T lymphocyte expresses a T-cell receptor (TCR) that recognizes cognate antigen and controls T-cell activation, different T cells bearing the same TCR can be functionally distinct. Each TCR is a heterodimer, and both alpha- and beta-chains contribute to determining TCR antigen specificity. Here we present a methodology enabling integration of information about TCR specificity with information about T cell function. This method involves sequencing of TCR alpha and TCR beta genes, and amplifying functional genes characteristic of different T cell subsets, in single T cells. Because this approach retains information about individual TCR alpha-TCRb beta pairs, TCRs of interest can be expressed and used in functional studies, for antigen discovery, or in therapeutic applications. We apply this approach to study the clonal ancestry and differentiation of T lymphocytes infiltrating a human colorectal carcinoma.

Aim: We carried out an association study between T-cell receptor beta polymorphism (TCRB) and endometriosis to investigate the difference in allelic frequency. Polymorphisms in T-cell receptor genes can provide important information for the study of the immune response and autoimmune diseases; indeed, rs1800907, a very common single nucleotide polymorphism (SNP) of the TCRB, has been extensively studied in autoimmune diseases in the 1990s using Southern blot analysis and more recently polymerase chain reaction (PCR) and sequencing. An autoimmune etiology for endometriosis has been strongly suggested for the presence of antibodies against endometrium, high rates of autoimmune disorders and associated atopic diseases. Material and Methods: We investigated 70 patients with endometriosis and 120 controls. DNA of patients and controls was studied by PCR followed by restriction digestion and sequencing to determine genotype and presence of linkage disequilibrium (LD). Statistical analysis was carried out using STATA Routine GENHW (StataCorp, College Station, TX, USA) for estimation of Hardy-Weinberg equilibrium and test power calculation. The difference of allele distribution between patients and controls was calculated according to Pearson's and Fisher's tests. Test power for the estimation of linkage disequilibrium is low (0.16). Results: We performed an association study of the SNP rs1800907 of TCRB between 70 patients with endometriosis and 120 controls, and did not find any significant difference (chi(2) = 0.27 and P = 0.87). Fisher's test confirmed a P-value of 0.872. Conclusion: Our study does not suggest an evidential and major involvement of TCRB in the pathogenesis of endometriosis in an Italian population in a small case control study.