Launois P Gumy A Himmelrich H Locksley RM Röcken M Louis JA 2002 Rapid production of IL-4 by Leishmania homolog of mammalian RACK1 (LACK)-reactive CD4(+) T cells expressing the V beta 4-V alpha 8 TCR chains has been shown to drive aberrant Th2 cell development and susceptibility to Leishmania major in BALB/c mice. In contrast, mice from resistant strains fail to express this early IL-4 response. However, administration of either anti-IL-12 or -IFN-gamma at the initiation of infection allows the expression of this early IL-4 response in resistant mice. In this work we show that Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells also expressing the V beta 4-V alpha 8 TCR chains are the source of the early IL-4 response to L. major in resistant mice given anti-IL-12 or -IFN-gamma Abs only at the onset of infection. Strikingly, these cells were found to be required for the reversal of the natural resistance of C57BL/6 mice following a single administration of anti-IL-12 or -IFN-gamma Abs. Together these results suggest that a deficiency in mechanisms capable of down-regulating the early IL-4 response to L. major contributes to the exquisite susceptibility of BALB/c mice to L. major. application/pdf https://sonar.ch/global/documents/277858 eng info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.168.9.4628 info:eu-repo/semantics/altIdentifier/pmid/11971011 info:eu-repo/semantics/openAccess Journal of immunology (Baltimore, Md. : 1950). - 2002 Animals Antibodies Antigens, Protozoan CD4-Positive T-Lymphocytes Cell Differentiation Cells, Cultured Cytokines Disease Progression Female Interferon-gamma Interleukin-12 Interleukin-4 Kinetics Leishmania major Leishmaniasis, Cutaneous Mice Mice, Inbred BALB C Mice, Inbred C57BL Protozoan Proteins RNA, Messenger Receptors, Antigen, T-Cell, alpha-beta Th2 Cells Rapid IL-4 production by Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells in resistant mice treated once with anti-IL-12 or -IFN-gamma antibodies at the onset of infection with Leishmania major instructs Th2 cell development, resulting in nonhealing lesions. http://purl.org/coar/resource_type/c_6501