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,
*
Center for Pulmonary and Infectious Disease Control, and Departments of
Cell Biology and
Medicine, University of Texas Health Center, Tyler, TX 75710;
§
Department of Inflammation/Autoimmune Diseases, Hoffmann-La Roche, Nutley, NJ 07110; and
¶
Department of Pathology, Nanjing Medical University, Nanjing, People’s Republic of China
To determine whether the Th1 response in tuberculosis correlated
with IL-12R expression, we measured expression of the IL-12Rß1 and
IL-12Rß2 subunits, as well as IL-12Rß2 mRNA expression in
tuberculosis patients and healthy tuberculin reactors. In tuberculosis
patients, IFN-
production by Mycobacterium
tuberculosis-stimulated PBMC was reduced, the percentages of T
cells expressing IL-12Rß1 and IL-12Rß2 were significantly
decreased, and IL-12Rß2 mRNA expression was also markedly reduced. In
contrast, in pleural fluid and lymph nodes at the site of disease in
tuberculosis patients, in which IFN- production is enhanced,
IL-12Rß2 mRNA expression was also increased. In M.
tuberculosis-stimulated peripheral blood T cells from
tuberculosis patients, anti-IL-10 and anti-TGF-ß enhanced
IL-12Rß1 and IL-12Rß2 expression, and IFN- production. In
M. tuberculosis-stimulated peripheral blood T cells from
healthy tuberculin reactors, recombinant IL-10 and TGF-ß reduced
IL-12Rß1 and IL-12Rß2 expression, as well as IFN- production. In
combination with prior studies showing increased production of TGF-ß
by blood monocytes from tuberculosis patients, this suggests that
increased TGF-ß production is the underlying abnormality that reduces
IL-12Rß1 and IL-12Rß2 expression in tuberculosis. Our findings
provide evidence that IL-12R expression correlates well with IFN-
production in human tuberculosis, and that expression of IL-12Rß1 and
IL-12Rß2 may play a central role in mediating a protective Th1
response.
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