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Author Notes:

E-mail: suzanne-cassel@uiowa.edu

CC and JRJ contributed equally to this work.

Conceived and designed the experiments: CC JRJ CFB FSS SLC.

Performed the experiments: CC JRJ NJ SH CPS JJS.

Analyzed the data: CC JRJ FSS SLC SH AKO.

Contributed reagents/materials/analysis tools: YI DMS.

Wrote the paper: FSS SLC.

We thank David Mosser and William Nauseef for helpful discussion and critical review of this manuscript; Richard Flavell, David Chaplin, and Millennium Pharmaceuticals for providing knockout mice; and Vickie Knepper-Adrian for technical assistance.

The authors have declared that no competing interests exist.

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Research Funding:

This work was supported by National Institutes of Health grants R01 AI104706 (S.L.C.), T32 AI007485 (J.R.J.), and T32 AI007511 (S.H.); an Asthma and Allergy Foundation of America fellowship (S.L.C.); an American Lung Association/The American Academy of Allergy, Asthma & Immunology Foundation Allergic Respiratory Disease Award (S.L.C.); and a Bolsista da CAPES Scholarship, 2790-14-9 (C.P.S.).

Keywords:

  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
  • CD4(+) T-CELLS
  • MICE DEFICIENT
  • AIRWAY INFLAMMATION
  • NLRP3 INFLAMMASOME
  • ADAPTIVE IMMUNITY
  • DENDRITIC CELLS
  • RECEPTOR
  • MACROPHAGES
  • CASPASE-1
  • Immune response
  • Immune complex
  • Immune suppression
  • Cytokines
  • T cells
  • Inflammation
  • Enzyme-linked immunoassays
  • Dendritic cells

Immune Complexes Indirectly Suppress the Generation of Th17 Responses In Vivo

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Journal Title:

PLoS ONE

Volume:

Volume 11, Number 3

Publisher:

, Pages e0151252-e0151252

Type of Work:

Article | Final Publisher PDF

Abstract:

The precise context in which the innate immune system is activated plays a pivotal role in the subsequent instruction of CD4+ T helper (Th) cell responses. Th1 responses are downregulated when antigen is encountered in the presence of antigen-IgG immune complexes. To assess if Th17 responses to antigen are subject to similar influences in the presence of immune complexes we utilized an inflammatory airway disease model in which immunization of mice with Complete Freund's Adjuvant (CFA) and ovalbumin (Ova) induces a powerful Ova-specific Th1 and Th17 response. Here we show that modification ofthat immunization with CFA to include IgG-Ova immune complexes results in the suppression of CFA-induced Th17 responses and a concurrent enhancement of Ova-specific Th2 responses. Furthermore, we show the mechanism by which these immune complexes suppress Th17 responses is through the enhancement of IL-10 production. In addition, the generation of Th17 responses following immunization with CFA and Ova were dependent on IL-1 a but independent of NLRP3 inflammasome activation. Together these data represent a novel mechanism by which the generation of Th17 responses is regulated.

Copyright information:

© 2016 Ciraci et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).

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