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The Journal of Immunology, Vol 159, Issue 7 3434-3443, Copyright © 1997 by American Association of Immunologists
ARTICLES |
P Kropf, R Etges, L Schopf, C Chung, J Sypek and I Muller
Department of Biological Sciences, University of Notre Dame, IN 46556, USA.
IL-4 drives polarized Th2 responses, and differentiating Th2 cells down- regulate their sensitivity to IL-12. Therefore, the failure of BALB/c mice to heal Leishmania major infection could be due to an IL-4- dependent biased Th2 response or to a reduced capacity of Leishmania- specific Th cells to respond to IL-12. We examined the ability of CD4+ Th cells from L. major-infected wild-type and IL-4-deficient BALB/c mice to respond to IL-12. We show that the inability of normal and IL-4- deficient BALB/c mice to heal L. major infections is due to their inability to generate effective Th1 responses and not to persistent IL- 4-dominated Th2 responses. Redirection of immune responses in vivo by administration of IL-12 or anti-CD4 mAb treatment in the early phase of infection (+/-12 days) allows both normal and IL-4-deficient BALB/c mice to heal their lesions by allowing them to develop an efficient Th1 response regardless of the presence or the absence of IL-4. Finally, on a population level, Ag-specific Th cells from infected animals induced to heal display a strongly elevated response to IL-12.
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