Expression of T cell receptors TcR1 (gamma/delta) and TcR2 (alpha/beta) in the human intestinal mucosa

Abstract

Cryostat sections of normal human adult gastrointestinal mucosae were studied by double-label immunofluorescence with antibodies to CD3, CD4, CD8, CD5 and CD6, in parallel with antibodies fF1 and TCR61 against fl-chains and 6-chains of the T-cell receptor (TcR) types TcR2 (a/f) and TcRl (y/6), respectively. Virtually no TcRl + were found within the lamina propria. In the epithelial compartment, TcR1 + cells were infrequent: in the small bowel, -2% of T cells were TcR1 + . In the colonic epithelium, the percentage of T cells expressing y/6-chains was higher, with a mean value approximating 15-20%, although this apparently large percentage increase compared with small bowel reflects in part a much lower density ofcolonic IEL, as absolute numbers ofTCRbI + cells were comparable. Of the TcRl + population, about half were CD4-CD8-'double negatives' and the remainder were CD8+. TcRl + cells were also CD5-CD6-, irrespective of expression of CD8. No CD4+ cells expressing TcRl were observed: essentially all CD4+ cells were fF1+, with some variability of labelling intensity. Approximately 30-50% of the CD8+ subset expressed the PF1 antigen strongly. However, in the remaining TcRl -CD8+ cells, which were all of the CD5-CD6phenotype, expression of the flF1 antigen was only detectable when streptavidin and biotin conjugates were used for amplification of labelling. Thus, the CD8+ CD5subset, a prominent population of the epithelial compartment of the small bowel, was either TcR2dUII in the majority or TcRl + in a minority. Our data imply that y/6 TcRl cells may be actively excluded from intestinal lamina propria, and that any preferential localization that does occur is limited and is rather a feature of the colonic mucosa, rather than the small bowel.

CD8+αβ+ T Cells That Lack Surface CD5 Antigen Expression Are a Major Lymphotactin (XCL1) Source in Peripheral Blood Lymphocytes

“…The size of this subset in the different lymphoid compartments was small; in peripheral blood, according to previously published data (41,42), the percentage of CD3 ϩ CD8 ϩ CD5 Ϫ cells within the CD8-expressing population was 5.2 Ϯ 2.8 (range, 10.2-1.0); the size of this subset was significantly lower in lymph nodes (1.3 Ϯ 0.8; range, 2.5-0.5; p Ͻ 0.01, according to the Mann-Whitney test) and tonsils (3.5 Ϯ 3.0; range, 7.9 -1.0); in these latter, probably due to the small number of samples examined, the difference from PBMC was not significant ( p ϭ 0.43).…”

Small intestinal CD8+TCRγδ+NKG2A+ intraepithelial lymphocytes have attributes of regulatory cells in patients with celiac disease

“…The frequency of TCRγδ + IELs in human intestinal epithelium ranges from 2% to 40%, depending on the segment of bowel sampled (27)(28)(29)(30). Several reports have shown that the frequency of TCRγδ + IELs is increased in the small intestine of patients with CD compared with healthy individuals (8)(9)(10)(11).…”

The γδ T cell repertoire in Graves' disease and multinodular goitre

“…although the role they play in the immune system is still unclear [1], Postulated functions include immunity to mycobacterial antigens and heal shock proteins, epithelial immune surveillance and immunorcgulation [1 3). The development of the -, <^ TCR repertoire is ordered, with expression of certain variable region combinations at dilTercnt times in ontogeny [1], V(')l • ceils constitute a major fraction of y6 T cells in several epithelial sites [1,[4][5][6][7][8], although the localization ofyt^ Tcell subsets to epithelial sites is less protiotmccd ihan fn mice fl], yS T cc\h expressing cevXd 'in receptors are over-represented in the rheumatoid synovium [I,y-I4] and in active multiple sclerosis lesions 11,15.16], It is therefore possible that yd T cells have a general role in autoimmune diseases [1], Graves' disease (GD) is eaused by autoantibodies stimulating the thyroid stimulating hormone receptor, although the initiating factors remain unknown. Heat shock proteins, known y6 T cell antigens, may play a role in the pathogenesis of GD [17.18], and -/tiTcells have been reported to be increased in the Correspondence: A, P, Weetman.…”