Distribution of T cells bearing different forms of the T cell receptor γ/δ in normal and pathological human tissues

Frozen sections from normal and pathologic human tissues were immunostained by the APAAP technique with three mAb directed against different epitopes of the TCRγδ; TCRδ1 which binds to all cells bearing the TCRγδ; BB3 and δTCS1 which, by immunoprecipitation studies, appear to react respectively with the disulfide-linked and nondisulfide-linked form of the TCRγδ. In normal thymus, TCRδ1⁺ cells accounted for approximately 2% of the CD3⁺ thymocytes and were about three times more numerous in the medulla than in the cortex. TCRδ1⁺ cells were mostly constituted by the δTCS1 reactive subset (average ratio δTCS1/BB3: 3.7). In the tonsil, the TCRδ1⁺ cells (about 3% of CD3⁺ elements) were mainly located in the interfollicular area, where they frequently tended to arrange around high endothelium venules. In most samples, TCRδ1⁺ cells were distributed beneath to the tonsil epithelium. Unlike thymus, the majority of TCRδ1⁺ cells were usually constituted by the BB3-reactive subset (average BB3/δTCS1 ratio: 2.0). A similar predominance of BB3⁺ over δTCS1⁺ cells was also observed in normal peripheral blood. The spleen was the organ with the highest concentration of TCRδ1⁺ cells that, like in the thymus, were mostly represented by δTCS1⁺ elements. Noteworthy, the TCRδ1⁺ cells were preferentially located in the splenic sinusoids while TCRαβ-bearing lymphocytes mostly occupied the periarteriolar sheaths of penicillary arteries. The majority of neoplastic T cell proliferations studied lacked to express the TCRγδ. Two cases of βF1^- (TCR αβ^-) T lymphoblastic lymphoma, however, were TCRγδ⁺ (δTCS1⁺/BB3^-). Both of them showed a stage II cortical phenotype, e.g., CD1⁺/CD3⁺/CD4⁺/CD8⁺/TCRδ1⁺. Among inflammatory conditions, an increase of BB3⁺ cells was observed in close association with necrotic areas in cases of Kikuchi's and tuberculous lymphadenitis. The significance of this finding is under study.