CD19 and CD22 regulate a B lymphocyte signal transduction pathway that contributes to autoimmunity.

Published

Journal Article

The fate of B lymphocytes is dependent on intrinsic and B cell antigen receptor (BCR)-induced signals. These signals are modified and interpreted by other cell-surface molecules such as CD19 and CD22 that govern mature B cell activation. This review assesses our current understanding of how CD19 and CD22 regulate B lymphocyte signaling and how alterations in these response-regulators contribute to autoimmunity in mice and humans. We propose that CD19 functions as a specialized adapter protein that regulates B lymphocyte signaling and autoantibody production. Overexpression of CD19 by B cells in systemic sclerosis patients correlates with autoantibody production and transgenic mice that overexpress CD19 produce similar autoantibodies. CD19 establishes a novel Src-family kinase activation loop that regulates basal signal transduction thresholds in resting B cells and amplifies Src-family kinase activation following BCR ligation. Reciprocally, CD22 is a potent regulator of CD19 function. These observations provide insight into how CD19 and CD22 govern the molecular ordering and intensity of signals transduced in B cells that may contribute to autoimmunity.

Full Text

Duke Authors

Cited Authors

  • Tedder, TF; Sato, S; Poe, JC; Fujimoto, M

Published Date

  • March 2000

Published In

Volume / Issue

  • 49 / 1

Start / End Page

  • 1 - 13

PubMed ID

  • 10750375

Pubmed Central ID

  • 10750375

Electronic International Standard Serial Number (EISSN)

  • 1880-1293

International Standard Serial Number (ISSN)

  • 0022-9717

Language

  • eng