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Gene expression program of AM-14 B cells stimulated through the B cell receptor (BCR) and/or Toll-like receptors (TLR)

ABSTRACT: We have previously shown that rheumatoid factors (RF) produced by Fas-deficient autoimmune-prone mice typically bind autologous IgG2a with remarkably low affinity. Nevertheless, B cells representative of this RF population proliferate vigorously in response IgG2a/chromatin immune complexes through a mechanism dependent on the sequential engagement of the BCR and Toll-like receptor 9 (TLR9). To more precisely address the role of both receptors in this response, we analyzed the signaling pathways activated in AM14 B cells stimulated with these complexes. We found that the BCR not only serves to direct the chromatin complex to an internal compartment where it can engage TLR9 but also transmits a suboptimal signal that in combination with the signals emanating from TLR9 leads to NF?B activation and proliferation. Importantly, engagement of both receptors leads to the upregulation of a group of gene products, not induced by the BCR or TLR9 alone, that include IL-2. These data indicate that autoreactive B cells, stimulated by a combination of BCR and TLR9 ligands, acquire functional properties that may contribute to the activation of additional cells involved in the autoimmune disease process. Keywords: cell stimulation

ORGANISM(S): Mus musculus

PROVIDER: GSE6674 | GEO | 2007/12/01

SECONDARY ACCESSION(S): PRJNA98613

REPOSITORIES: GEO

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Transcription profiling of mouse AM-14 B cells stimulated through the B cell receptor (BCR) and/or Toll-like receptors (TLR)

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2008-06-15 | E-GEOD-6674 | biostudies-arrayexpress

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2014-05-21 | E-GEOD-47147 | biostudies-arrayexpress

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