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- W2102821093 abstract "The adaptors DOCK8 and MyD88 have been linked to serological memory. Here we report that DOCK8-deficient patients had impaired antibody responses and considerably fewer CD27(+) memory B cells. B cell proliferation and immunoglobulin production driven by Toll-like receptor 9 (TLR9) were considerably lower in DOCK8-deficient B cells, but those driven by the costimulatory molecule CD40 were not. In contrast, TLR9-driven expression of AICDA (which encodes the cytidine deaminase AID), the immunoglobulin receptor CD23 and the costimulatory molecule CD86 and activation of the transcription factor NF-κB, the kinase p38 and the GTPase Rac1 were intact. DOCK8 associated constitutively with MyD88 and the tyrosine kinase Pyk2 in normal B cells. After ligation of TLR9, DOCK8 became tyrosine-phosphorylated by Pyk2, bound the Src-family kinase Lyn and linked TLR9 to a Src-kinase Syk-transcription factor STAT3 cascade essential for TLR9-driven B cell proliferation and differentiation. Thus, DOCK8 functions as an adaptor in a TLR9-MyD88 signaling pathway in B cells." @default.
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- W2102821093 date "2012-05-13" @default.
- W2102821093 modified "2023-10-17" @default.
- W2102821093 title "DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation" @default.
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- W2102821093 doi "https://doi.org/10.1038/ni.2305" @default.
- W2102821093 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3362684" @default.
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