TLR and B Cell Receptor Signals to B Cells Differentially Program Primary and Memory Th1 Responses to Salmonella enterica | Zendy

Tom A. Barr | Zendy; Sheila Brown | Zendy; Pietro Mastroeni | Zendy; David Gray | Zendy

Open Access

TLR and B Cell Receptor Signals to B Cells Differentially Program Primary and Memory Th1 Responses to Salmonella enterica

Author(s) -

Tom A. Barr,

Sheila Brown,

Pietro Mastroeni,

David Gray

Publication year - 2010

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1001431

Subject(s) - biology , salmonella enterica , b cell , breakpoint cluster region , b cell receptor , effector , microbiology and biotechnology , salmonella , immunology , naive b cell , receptor , t cell , immune system , antigen presenting cell , antibody , genetics , bacteria

Protective Th1 responses to Salmonella enterica do not develop in the absence of B cells. Using chimeric mice, we dissect the early (innate) and late (cognate) contributions of B cells to Th programming. B cell-intrinsic MyD88 signaling is required for primary effector Th1 development, whereas Ag-specific BCR-mediated Ag presentation is necessary for the development of memory Th1 populations. Programming of the primary T cell response is BCR/B cell MHC II independent, but requires MyD88-dependent secretion of cytokines by B cells. Chimeras in which B cells lack IFN-gamma or IL-6 genes make impaired Th1 or Th17 responses to Salmonella.

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