IL-17A induces CCL28, supporting the chemotaxis of IgE-secreting B cells

Int Arch Allergy Immunol. 2011;156(1):51-61. doi: 10.1159/000322178. Epub 2011 Mar 29.


Background: Atopic asthma is an allergic disease typically associated with T(H)2 cytokines. IL-17A is also associated with asthma, through the induction of chemokines. Mucosal CCL28 concentrations correlate with cellular recruitment to inflamed airways and support migration of IgA(+) B cells. Here, a link between IL-17A, CCL28 and IgE-secreting B cell chemotaxis is examined.

Methods: Primary human airway cells and the airway epithelial line A549 were used to characterize IL-17A receptor expression and the effect of IL-17A on CCL28 transcription and translation. B cells, differentiated to IgE+ cells ex vivo, were assessed for CCR10 surface expression and chemotaxis to CCL28 by flow cytometry, transwell migration and ELISpot.

Results: Human airway epithelium expressed both IL-17RA and IL-17RC, and was responsive to IL-17A stimulation. Cultured human IgE+ B cells expressed surface CCR10 and displayed CCR10-dependent chemotaxis towards recombinant CCL28. Enhanced levels of CCL28 were observed upon A549 cell incubation with IL-17A, and this up-regulation significantly increased the migration of IgE+ antibody-secreting B cells. The specificity of chemotaxis was confirmed by migration blockade in the presence of anti-CCL28 or anti-CCR10.

Conclusions: This work identifies a novel chemokine for the migration of IgE+ B cells, in addition to characterizing induction of CCL28 by IL-17A. Taken together the results presented here propose a new role for IL-17A in the allergic airways, linking this cytokine with the recruitment of IgE+ antibody-secreting B cells, via the induction of CCL28. These observations justify further in vivo studies of larger cohorts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Asthma / immunology
  • Asthma / metabolism
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • B-Lymphocytes / physiology*
  • Cell Line
  • Cells, Cultured
  • Chemokines, CC / genetics
  • Chemokines, CC / metabolism*
  • Chemotaxis, Leukocyte / physiology*
  • Humans
  • Hypersensitivity / genetics
  • Hypersensitivity / immunology
  • Hypersensitivity / metabolism
  • Immunoglobulin E / metabolism*
  • Interleukin-17 / immunology*
  • Interleukin-17 / metabolism
  • Receptors, CCR10 / biosynthesis
  • Receptors, CCR10 / genetics


  • CCL28 protein, human
  • Chemokines, CC
  • Interleukin-17
  • Receptors, CCR10
  • Immunoglobulin E