Asthma‐associated long tslp inhibits the production of iga

Dorianne van Heerden, Robert S. van Binnendijk, Samantha A.M. Tromp, Huub F.J. Savelkoul, R.J.J. van Neerven, Gerco den Hartog*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Thymic stromal lymphopoietin (TSLP) contributes to asthmatic disease. The concentrations of protective IgA may be reduced in the respiratory tract of asthma patients. We investigated how homeostatic short TSLP (shTSLP) and asthma‐associated long TSLP (loTSLP) regulate IgA production. B cells from healthy donors were stimulated in the presence or absence of shTSLP or loTSLP; the concentrations of IgA, IgM, IgE, and IgG antibodies were determined in cell culture supernatants; and B cells were analyzed by flow cytometry. LoTSLP, but not shTSLP, suppressed the secretion of IgA but not of IgE. The type 2 cytokine IL‐4, which in addition to loTSLP contributes to asthmatic disease, did not affect the production of IgA or the frequency of IgA+ B cells. Instead, IL‐4 increased IgG production, especially of the subclasses IgG2 and IgG4. LoTSLP inhibited IgA secretion by sorted memory B cells but not by naïve B cells. Although loTSLP inhibited IgA production, the vitamin A metabolite retinoic acid promoted the secretion of IgA, also in the presence of loTSLP, suggesting that vitamin A may promote IgA production in asthma. Our data demonstrate that asthma‐associated loTSLP negatively regulates the secretion of IgA, which may negatively impact the surveillance of mucosal surfaces in asthma.

Original languageEnglish
Article number3592
JournalInternational Journal of Molecular Sciences
Volume22
Issue number7
DOIs
Publication statusPublished - 30 Mar 2021

Keywords

  • Asthma
  • IgA
  • IgE
  • IgG4
  • IL‐13
  • IL‐4
  • Memory B cells
  • Short and long TSLP

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