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,,
*
Department of Medicine,
Division of Dermatology, and
Department of Microbiology and Immunology, University of California School of Medicine, Los Angeles, CA 90095; and
§
Section of Dermatology, University of Southern California School of Medicine, Los Angeles, CA 90033
The interaction of CD40 ligand (CD40L) expressed by activated T
cells with CD40 on macrophages has been shown to be a potent stimulus
for the production of IL-12, an obligate signal for generation of Th1
cytokine responses. The expression and interaction of CD40 and CD40L
were investigated in human infectious disease using leprosy as a model.
CD40 and CD40L mRNA and surface protein expression were predominant in
skin lesions of resistant tuberculoid patients compared with the highly
susceptible lepromatous group. IL-12 release from PBMC of tuberculoid
patients stimulated with Mycobacterium leprae was
partially inhibited by mAbs to CD40 or CD40L, correlating with
Ag-induced up-regulation of CD40L on T cells. Cognate recognition of
M. leprae Ag by a T cell clone derived from a
tuberculoid lesion in the context of monocyte APC resulted in
CD40L-CD40-dependent production of IL-12. In contrast, M.
leprae-induced IL-12 production by PBMC from lepromatous
patients was not dependent on CD40L-CD40 ligation, nor was CD40L
up-regulated by M. leprae. Furthermore, IL-10, a
cytokine predominant in lepromatous lesions, blocked the IFN-
up-regulation of CD40 on monocytes. These data suggest that T cell
activation in situ by M. leprae in tuberculoid leprosy
leads to local up-regulation of CD40L, which stimulates CD40-dependent
induction of IL-12 in monocytes. The CD40-CD40L interaction, which is
not evident in lepromatous leprosy, probably participates in the
cell-mediated immune response to microbial
pathogens.
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