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Immunology of susceptibility and resistance to Leishmania major reviewed.

Vaccine Weekly

| March 12, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 MAR 12 - (NewsRx.com & NewsRx.net) -- A review covering the immunology of susceptibility and resistance to Leishmania major has been published.

"Established models of T-helper-2-cell dominance in BALB/c mice infected with Leishmania major - involving the early production of interleukin-4 (IL-4) by a small subset of Leishmania-specific CD4+ T cells - have been refined by accumulating evidence that this response is not sufficient and, under some circumstances, not required to promote susceptibility," researchers in the United States report.

"In addition, more recent studies in L. major-resistant mice have revealed complexities in the mechanisms responsible for acquired immunity, which necessitate the redesign of vaccines against Leishmania and other pathogens that require sustained cell-mediated immune responses" said David Sacks and Nancy Noben-Trauth at the National Institute of Allergy and Infectious Diseases. "The early production of IL-4 by an oligoclonal population of CD4+ T cells that recognize the Leishmania antigen LACK (Leishmania homologue of receptors for activated C kinase) is responsible, at least in part, for T helper 2 (Th2)-cell polarization and susceptibility to L. major infection in BALB/c mice."

The investigators reported, "On the basis of studies in anti-IL-12 antibody-treated or IL-12-knockout resistant-background mice, and in BALB/c mice treated with IL-12 at the time of challenge, it seems that the onset of IL-12 production by dendritic cells (DCs) is key to the redirection of the T-cell response and the development of acquired resistance. Selective loss of IL-12 signaling owing to ...

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