AUTHOR=Tran Giang T. , Wilcox Paul L. , Dent Lindsay A. , Robinson Catherine M. , Carter Nicole , Verma Nirupama D. , Hall Bruce M. , Hodgkinson Suzanne J. 

TITLE=Interleukin-5 Mediates Parasite-Induced Protection against Experimental Autoimmune Encephalomyelitis: Association with Induction of Antigen-Specific CD4+CD25+ T Regulatory Cells

JOURNAL=Frontiers in Immunology

VOLUME=Volume 8 - 2017

YEAR=2017

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2017.01453

DOI=10.3389/fimmu.2017.01453

ISSN=1664-3224

ABSTRACT=Objective.  To examine if the protective effect of parasite infection on Experimental Autoimmune Encephalomyelitis (EAE) was due to interleukin-5, a cytokine produced by a Type-2 response that induces eosinophilia. We hypothesise that in parasite infections IL-5 also promotes expansion of antigen-specific T regulatory cells that control autoimmunity.   
Methods.  Nippostrongylus brasiliensis larvae were used to infect Lewis rats prior to induction of EAE by myelin basic protein.  Animals were sham-treated, or given blocking monoclonal antibodies to interleukin 4 or 5 or to deplete CD25+T cells.  Reactivity of CD4+CD25+T regulatory cells from these animals was examined.
Results. Parasite infected hosts had reduced severity and length of EAE.  The beneficial effect of parasitic infection was abolished with an anti-IL-5 or an anti-CD25 monoclonal antibody, but not anti-IL-4 monoclonal antibody.  Parasite infected animals with EAE developed antigen-specific CD4+CD25+T regulatory cells earlier than EAE controls and these expressed more Il5ra than controls.  Treatment with IL-5 also reduced the severity of EAE and induced Il5ra expressing CD4+CD25+T regulatory cells.  
Interpretation.  The results of this study suggested that IL-5 produced by the Type-2 inflammatory response to parasite infection promoted induction of autoantigen-specific CD25+Il5ra+T regulatory cells that reduced the severity of autoimmunity. Such a mechanism may explain the protective effect of parasite infection in patients with multiple sclerosis where eosinophilia is induced by IL-5, produced by the immune response to parasites.