02346nas a2200385 4500000000100000008004100001260001600042653001800058653002000076653001100096653001800107653001800125653001200143653002600155653002800181653002500209653003000234653002700264653002900291653001900320653001800339100001600357700001500373700001400388700001500402700001500417700001800432700001200450700001500462245006700477300001200544490000800556520138200564022001401946 1995 d c1995 Mar 1510aBase Sequence10aCells, Cultured10aHumans10aInterleukin-710aKeratinocytes10aleprosy10aLymphocyte Activation10aMolecular Sequence Data10aMycobacterium leprae10apolymerase chain reaction10aReceptors, Interleukin10aReceptors, Interleukin-710aRNA, Messenger10aT-Lymphocytes1 aSieling P A1 aSakimura L1 aUyemura K1 aYamamura M1 aOliveros J1 aNickoloff B J1 aRea T H1 aModlin R L00aIL-7 in the cell-mediated immune response to a human pathogen. a2775-830 v1543 a

The goal of the present study was to investigate the role of IL-7 in regulating immune responses to infection. Leprosy provides a model for understanding human immune responses to infection; the disease presents as a spectrum in which the clinical manifestations correlate with the levels of cell-mediated immunity to the pathogen, Mycobacterium leprae. To determine whether IL-7 is produced at the site of infection in leprosy, we used the PCR to measure IL-7 and IL-7R mRNA in skin lesions. IL-7 mRNA was more strongly expressed in the tuberculoid form of the disease, in which the infection is limited (mean cpm = 48 +/- 8; n = 11), as compared with the progressive lepromatous form (17 +/- 2; n = 11). IL-7R mRNA, both membrane-bound and soluble forms, were also more strongly expressed in tuberculoid lesions, although these differences were not as striking as those for IL-7. The cellular source of IL-7 included Ag-stimulated monocytes and IFN-gamma-induced keratinocytes. M. leprae-induced PBMC responses in tuberculoid patients involved up-regulation of IL-7 and IL-7R mRNA and was IL-7 dependent. In contrast, M. leprae did not induce IL-7 mRNA in lepromatous patients, and their T cell responses were weakly augmented by rIL-7. These data suggest that IL-7, produced at the site of disease, contributes to the cell-mediated immune response to human pathogens.

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