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Responding to infection and apoptosis — a task for T H 17 cells
Author(s) -
Brereton Corinna F.,
Blander J. Magarian
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05747.x
Subject(s) - immunology , antigen presenting cell , biology , citrobacter , t cell , immune system , apoptosis , microbiology and biotechnology , cytokine , interleukin 3 , innate immune system , enterobacteriaceae , biochemistry , escherichia coli , gene
Two of the critical cytokines required for the differentiation of T helper 17 (T H 17) cells from naive CD4 T cells are transforming growth factor‐beta (TGF‐β) and interleukin‐6 (IL‐6). Innate recognition of apoptotic cells in the presence of Toll‐like receptor engagement directs the simultaneous synthesis of these cytokines by antigen‐presenting cells (APCs), and as such provides a cytokine milieu that favors T H 17 cell induction. In this situation, APCs are activated in response to ligands derived from apoptotic cells, but also to those from the infecting pathogen. Induction of a T H 17 response against Citrobacter rodentium infection was dependent on the ability of Citrobacter to induce apoptosis of intestinal epithelial cells. In this review, we will discuss how simultaneous activation of inflammatory and noninflammatory pattern recognition receptors on APCs impacts T helper cell differentiation, and what relevance this effect has on the immune response generated against bacterial infections that cause host cell apoptosis.