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* Laboratory of Mycobacterial Immunity and Pathogenesis, Public Health Research Institute, Newark, NJ 07103;
Health Protection Agency, London, United Kingdom;
Center for AIDS Research, New York University New York, NY 10016; and
National Hansen’s Disease Programs Laboratory Research Branch, Louisiana State University, Baton Rouge, LA 70803
Leprosy presents with a clinical spectrum of skin lesions that span from strong Th1-mediated cellular immunity and control of bacillary growth at one pole to poor Ag-specific T cell immunity with extensive bacillary load and Th2 cytokine-expressing lesions at the other. To understand how the immune response to Mycobacterium leprae is regulated, human dendritic cells (DC), potent inducers of adaptive immune responses, exposed to M. leprae, Mycobacterium tuberculosis (Mtb), and Mycobacterium bovis bacillus Calmette-Guerin (BCG) were studied for their ability to be activated and to prime T cell proliferation. In contrast with Mtb and BCG, M. leprae did not induce DC activation/maturation as measured by the expression of selected surface markers and proinflammatory cytokine production. In MLR, T cells did not proliferate in response to M. leprae-stimulated DC. Interestingly, M. leprae-exposed MLR cells secreted increased Th2 cytokines as well as similar Th1 cytokine levels as compared with Mtb- and BCG-exposed cells. Gene expression analysis revealed a reduction in levels of mRNA of DC activation and maturation markers following exposure to M. leprae. Our data suggest that M. leprae does not induce and probably suppresses in vitro DC maturation/activation, whereas Mtb and BCG are stimulatory.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by American Leprosy Missions (to J.K.), the Heiser Program for Leprosy and Tuberculosis Research (to R.A.M.), and National Institutes of Health Grant R01AI022616 (to G.K.).
2 Address correspondence and reprint requests to Dr. Gilla Kaplan, Laboratory of Mycobacterial Immunity and Pathogenesis, Public Health Research Institute, 225 Warren Street, Newark, NJ 07103, E-mail address: kaplan{at}phri.org
3 Abbreviations used in this paper: T-lep, tuberculoid leprosy; 7-AAD, 7-aminoactinomycin D; BCG, bacillus Calmette-Guerin; CBA, cytometric bead array; DC, dendritic cell; DC-SIGN, DC-specific ICAM-3-grabbing nonintegrin; iDC, immature DC; L-lep, lepromatous leprosy; LAM, lipoarabinomannan; man-LAM, mannose-capped LAM; MC, maturation ("cocktail") mixture; MFI, mean fluorescence intensity; MOI, multiplicity of infection; Mtb, Mycobacterium tuberculosis; PGL-1, phenolic glycolipid 1.
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