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Front. Immunol. | doi: 10.3389/fimmu.2018.00401

Lyn, Lupus and (B) lymphocytes, a lesson on the critical balance of kinase signalling in immunity

 Erica J. Brodie1, Simona Infantino1, 2,  Michael Low2, 3, 4 and David M. Tarlinton1*
  • 1Monash University, Australia
  • 2University of Melbourne, Australia
  • 3Monash Health, Australia
  • 4Walter and Eliza Hall Institute of Medical Research, Australia

Systemic Lupus Erythematosus (SLE) is a progressive autoimmune disease characterised by increased sensitivity to self-antigens, auto-antibody production and systemic inflammation. B cells have been implicated in disease progression and as such represent an attractive therapeutic target. Lyn is a Src-family tyrosine kinase that plays a major role in regulating signalling pathways within B cells as well as other hematopoietic cells. Its role in initiating negative signalling cascades is especially critical as exemplified by Lyn-/- mice developing an SLE-like disease with plasma cell hyperplasia, underscoring the importance of tightly regulating signalling within B cells. This review highlights recent advances in our understanding of the function of the Src-family tyrosine kinase Lyn in B lymphocytes and its contribution to positive and negative signalling pathways that are dysregulated in autoimmunity

Keywords: lyn, SLE, cell signalling, SFK, B cell, BCR, Autoimmunity, lupus

Received: 08 Dec 2017; Accepted: 13 Feb 2018.

Edited by:

Marc Pellegrini, Walter and Eliza Hall Institute of Medical Research, Australia

Reviewed by:

Stamatis-Nick C. Liossis, University of Patras, Greece
Louis Justement, University of Alabama at Birmingham, United States
Aaron J. Marshall, University of Manitoba, Canada  

Copyright: © 2018 Brodie, Infantino, Low and Tarlinton. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. David M. Tarlinton, Monash University, Melbourne, Australia, david.tarlinton@monash.edu