Journal
JOURNAL OF IMMUNOLOGY
Volume 167, Issue 2, Pages 779-786Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.2.779
Keywords
-
Categories
Funding
- NIAID NIH HHS [AI22553, AI07118] Funding Source: Medline
- NIAMS NIH HHS [AR40312] Funding Source: Medline
Ask authors/readers for more resources
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 1L-12R beta1/IL-12R beta2 heterodimer, with the IL-12R beta2 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-12R beta2 was more highly expressed in tuberculoid lesions compared with lepromatous lesions. In contrast, IL-12R beta1 expression was similar in both tuberculoid and lepromatous lesions. The expression of IL-12R beta2 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-12R beta2 in lepromatous patients could be up-regulated by stimulation with M. tuberculosis. These data suggest that Th response to M. leprae determines IL-12R beta2 expression and function in host defense in leprosy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available