期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 6, 页码 3625-3634出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.6.3625
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Patients presenting with genetic deficiencies in IFNGR1, IFNGR2, IL-12B, and IL-12RB1 display increased susceptibility to mycobacterial infections. We analyzed in this group of patients the cross-talk between human CD4(+) T lymphocytes and dendritic cells (DCs) that leads to maturation of DC into producers of bioactive IL-12 and to activation of T cells into IFN-gamma producers. We found that this cross-talk is defective in all patients from this group. Unraveling the mechanisms underlying this deficiency, we showed that IL-12 signaling in T cells is required to induce expression of costimulatory molecules and secretion of IL-12 by DCs and that IFNGR expression is required on both DCs and CD4(+) T cells to induce IL-12 secretion by DCs. These data suggest that CD4(+) T cell-mediated activation of DCs plays a critical role in the defense against mycobacterial infections in humans.
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