4.6 Review

MicroRNA regulation of B cell receptor signaling*

Journal

IMMUNOLOGICAL REVIEWS
Volume 304, Issue 1, Pages 111-125

Publisher

WILEY
DOI: 10.1111/imr.13024

Keywords

AKT; BCR; MAPK; miRNA; NF-kappa B; PI3K

Categories

Funding

  1. NIH [R21AI110830, R21AI137752, R01HL125816]
  2. LEO Foundation [LF-OC-20-000351]
  3. Judith and Stewart Colton Center for Autoimmunity Pilot grant
  4. Binational Science Foundation
  5. NIAID [T32AI007180]
  6. NYU MSTP [T32GM007308]

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B lymphocytes play a central role in host immune defense, and their development and function are regulated by miRNAs. Studies have found that miRNAs are crucial for B cell development in the bone marrow and their subsequent population of the peripheral immune system, preventing autoimmunity by regulating downstream signaling of the B cell antigen receptor.
B lymphocytes play a central role in host immune defense. B cell receptor (BCR) signaling regulates survival, proliferation, and differentiation of B lymphocytes. Signaling through the BCR signalosome is a multi-component cascade that is tightly regulated and is important in the coordination of B cell differentiation and function. At different stages of development, B cells that have BCRs recognizing self are eliminated to prevent autoimmunity. microRNAs (miRNAs) are small single-stranded non-coding RNAs that contribute to post-transcriptional regulation of gene expression and have been shown to orchestrate cell fate decisions through the regulation of lineage-specific transcriptional profiles. Studies have identified miRNAs to be crucial for B cell development in the bone marrow and their subsequent population of the peripheral immune system. In this review, we focus on the role of miRNAs in the regulation of BCR signaling as it pertains to B lymphocyte development and function. In particular, we discuss the most recent studies describing the role of miRNAs in the regulation of both early B cell development and peripheral B cell responses and examine the ways by which miRNAs regulate signal downstream of B cell antigen receptor to prevent aberrant activation and autoimmunity.

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