Abstract
B-1 cells constitute a unique subset of B cells identified in several species including mice and humans. B-1 cells are further subdivided into B-1a and B-1b subsets as the former but not the later express CD5.The B-1a subset contributes to innate type of immune responses while the B-1b B cell subset contributes to adaptive responses. B-1 cell responses to B cell receptor (BCR) as well as Toll-like receptor (TLR) ligation are tightly regulated due to the cross-reactivity of antigen specific receptors on B-1 cells to self-antigens. B-1 cells are elevated in several autoimmune diseases. CD5 plays a major role in down regulation of BCR responses in the B-1a cell subset. Reduced amplification of BCR induced signals via CD19 and autoregulation of BCR and TLR responses by B-1 cell produced IL-10 appear to have a role in regulation of both B-1a and B-1b B cell responses. Siglec G receptors and Lyn kinase also regulate B-1 cell responses but their differential role in the two B-1 cell subsets is unknown.
Document Type
Article
Publication Date
12-17-2012
Digital Object Identifier (DOI)
http://dx.doi.org/10.3389/fimmu.2012.00372
Funding Information
This work was supported in part by NIH grants AI21490, AG05731, CA09357, and AI076956, a grant from Vice President for Research, University of Kentucky and a grant from Edward P. Evans Foundation to Subbarao Bondada.
Repository Citation
Sindhava, Vishal and Bondada, Subbarao, "Multiple Regulatory Mechanisms Control B-1 B Cell Activation" (2012). Microbiology, Immunology, and Molecular Genetics Faculty Publications. 2.
https://uknowledge.uky.edu/microbio_facpub/2
Notes/Citation Information
Published in Frontiers in Immunology, v. 3, article 372, p. 1-6.
© 2012 Sindhava and Bondada. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.