Endogenous IL-1R1 Signaling Is Critical for Cognate CD4 T Cell Help for Induction of In Vivo Type 1 and Type 2 Antipolysaccharide and Antiprotein Ig Isotype Responses to Intact Streptococcus pneumoniae, but Not to a Soluble

作者： Clifford M. Snapper , Goutam Sen , Quanyi Chen

DOI:

关键词: Priming (immunology) 、 Pathogen 、 Isotype 、 Antigen 、 Immunology 、 Streptococcus pneumoniae 、 In vivo 、 Biology 、 Endogeny 、 Immune system

摘要: MyD88 / mice secreted normal levels of IFN- and enhanced IL-5 IL-13. In contrast, IgG responses to a soluble, pneumococcal protein-PS conjugate, with or without adjuvant, showed little dependence on IL-1R1 CD4 T cell priming. These data are the first demonstrate nonredundant role for endogenous IL-1 in TD induction humoral immune an intact pathogen, although not pathogen-derived soluble suggesting that antigenic context is key determinant dependence. further suggest may be critical preserving Th2 function presence, but absence, MyD88-dependent signaling via TLRs. The Journal Immunology, 2006, 177: 6044‐6051.

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Endogenous IL-1R1 Signaling Is Critical for Cognate CD4 T Cell Help for Induction of In Vivo Type 1 and Type 2 Antipolysaccharide and Antiprotein Ig Isotype Responses to Intact Streptococcus pneumoniae, but Not to a Soluble

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Endogenous IL-1R1 Signaling Is Critical for Cognate CD4 T Cell Help for Induction of In Vivo Type 1 and Type 2 Antipolysaccharide and Antiprotein Ig Isotype Responses to Intact Streptococcus pneumoniae, but Not to a Soluble

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