The CCR6-CCL20 axis in humoral immunity and T-B cell immunobiology.

Affiliation

Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia; Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immunopharmacology, Ministry of Education, Engineering Technology Research Center of Anti-inflammatory and Immunodrugs in Anhui Province, Hefei, Anhui Province, People's Republic of China. Electronic address: [Email]

Abstract

Traditionally, chemokine immunobiology has focused on chemotaxis and the positioning of cells at sites of inflammation and within lymphoid organs. More recently, however, regulation of intricate immune responses has emerged as a function attributed to chemokines and their receptors. One such pair, CCR6 and its chemokine ligand CCL20, has been receiving interest for its potential role in the coordination and regulation of humoral immune responses and in particular, memory responses, at the cellular level. B cells up-regulate CCR6 after activation in secondary lymphoid organs; however, its function is still unclear. In an important insight, the CCR6-CCL20 chemokine axis has been implicated in the regulation of effective humoral responses - disruption of this pair led to an increased number of ineffective T-B cell conjugates and poorer quality antibodies. Interestingly, follicular helper T cells and their precursors also up-regulate CCR6; though, again, the precise purpose of this is yet to be discovered. The chemokine axis in relation to secondary lymphoid organ (SLO) structures will be briefly reviewed as well. With the implication of CCR6 and CCL20 in the pathogenesis of autoantibody-driven autoimmune diseases such as systemic lupus erythematosus, understanding the intricacies of this chemokine pair would be conducive to the development of appropriate, targeted therapeutic strategies.

Keywords

B cells,CCL20,CCR6,Chemokines,Humoral immunity,T cells,

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