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.
|Number of pages||9|
|Journal||Journal of Immunology|
|Publication status||Published - 1989|
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