02933nas a2200469 4500000000100000008004100001260001300042653002700055653002400082653001700106653001800123653003000141653004400171653002800215653001800243653002000261653002000281653001900301653001100320653001900331653002000350653002600370653004500396653001800441653004400459653002400503653001800527100002200545700002400567700001400591700001400605700001100619700002100630700001400651700001500665245010500680856007800785300001100863490000800874520156700882022001402449 2000 d c2000 Jun10aAntibodies, Monoclonal10aAntigens, Bacterial10aAntigens, CD10aAntigens, CD710aAntigens, Differentiation10aAntigens, Differentiation, T-Lymphocyte10aCell Adhesion Molecules10aCell Division10aCell Separation10aCells, Cultured10aFlow Cytometry10aHumans10aInterleukin-1010aLectins, C-Type10aLymphocyte Activation10aLymphocyte Function-Associated Antigen-110aMycobacterium10aReceptors, Antigen, T-Cell, gamma-delta10aSignal Transduction10aT-Lymphocytes1 aGonzález-Amaro R1 aPortales-Pérez D P1 aBaranda L1 aMoncada B1 aToro C1 aLópez-Briones S1 aEspitia C1 aMancilla R00aCo-stimulatory signals increase the reactivity of gammadelta T cells towards mycobacterial antigens. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905552/pdf/cei0120-0468.pdf a468-750 v1203 a
Although it has been shown that gammadelta T lymphocytes are able to react with different cell-associated or soluble antigens, the immune repertoire of these cells appears to be skewed to the recognition of mycobacterial antigens. We have studied the number and reactivity of gammadelta T cells towards several mycobacterial antigens in patients with tuberculosis and leprosy, as well as their healthy contacts and control individuals. We found an increased number of Vdelta2+ cells in healthy contacts (PPD+ and lepromin+) and tuberculoid leprosy patients. The gammadelta T cells from lepromatous leprosy showed a decreased response to all antigens tested, but some of these patients exhibited a significant response to the 30-kD glycoprotein of Mycobacterium tuberculosis. Interestingly, the reactivity of gammadelta T cells against mycobacterial antigens was significantly increased by costimulatory signals generated through CD7, LFA-1, CD50 and CD69 in all groups. However, signalling through CD69 did not enhance the responsiveness of gammadelta lymphocytes from lepromatous patients. On the other hand, the in vitro blockade of IL-10 with a specific antibody enhanced the cell proliferation of gammadelta lymphocytes from lepromatous leprosy patients, whereas exogenous IL-10 had an opposite effect in most individuals studied. These results suggest the potential role of different cell membrane receptors in the regulation of gammadelta T cell proliferation induced by mycobacteria, as well as the possible involvement of IL-10 in this phenomenon.
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