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*
Division of Dermatology, and
Department of Microbiology and Immunology, University of California School of Medicine, Los Angeles, CA 90095;
Section of Dermatology, University of Southern California School of Medicine, Los Angeles, CA 90033; and
Division of Hematology-Oncology, University of California School of Medicine, Los Angeles, CA 90095
The generation of cell-mediated immunity against intracellular
infection involves the production of IL-12, a critical cytokine
required for the development of Th1 responses. The biologic activities
of IL-12 are mediated through a specific, high affinity IL-12R composed
of an IL-12R
1/IL-12R2 heterodimer, with the IL-12R2 chain
involved in signaling via Stat4. We investigated IL-12R expression and
function in human infectious disease, using the clinical/immunologic
spectrum of leprosy as a model. T cells from tuberculoid patients, the
resistant form of leprosy, are responsive to IL-12; however, T cells
from lepromatous patients, the susceptible form of leprosy, do not
respond to IL-12. We found that the IL-12R2 was more highly
expressed in tuberculoid lesions compared with lepromatous lesions. In
contrast, IL-12R1 expression was similar in both tuberculoid and
lepromatous lesions. The expression of IL-12R2 on T cells was
up-regulated by Mycobacterium leprae in tuberculoid but
not in lepromatous patients. Furthermore, IL-12 induced Stat4
phosphorylation and DNA binding in M. leprae-activated T
cells from tuberculoid but not from lepromatous patients.
Interestingly, IL-12R2 in lepromatous patients could be up-regulated
by stimulation with M. tuberculosis. These data suggest
that Th response to M. leprae determines IL-12R2
expression and function in host defense in
leprosy.
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