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    Eosinophils are required to suppress Th2 responses in Peyer’s patches during intestinal infection by nematodes (2016)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Strandmark, J (WE 6)
    Steinfelder, S. (WE 6)
    Berek, C.
    Kühl, A.
    Rausch, S. (WE 6)
    Hartmann, S. (WE 6)
    Quelle
    Mucosal immunology; 10 — S. 661–672
    ISSN: 1933-0219
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://www.nature.com/mi/journal/vaop/ncurrent/full/mi201693a.html
    DOI: 10.1038/mi.2016.93
    Kontakt
    Institut für Immunologie und Molekularbiologie

    Robert-von-Ostertag-Str. 7-13
    Gebäude 35
    14163 Berlin
    Tel.+49 30 838 - 518 34 Fax.+49 30 838 451 834

    Abstract / Zusammenfassung

    Infections with enteric nematodes result in systemic type 2 helper T (Th2) responses, expansion of immunoglobulin (Ig)G1 antibodies, and eosinophilia. Eosinophils have a supportive role in mucosal Th2 induction during airway hyperreactivity. Whether eosinophils affect the local T-cell and antibody response in the gut-associated lymphoid tissue during enteric infections is unknown. We infected eosinophil-deficient ΔdblGATA-1 mice with the Th2-inducing small intestinal nematode Heligmosomoides polygyrus and found that parasite fecundity was decreased in the absence of eosinophils. A lack of eosinophils resulted in significantly augmented expression of GATA-3 and IL-4 by CD4+ T cells during acute infection, a finding strictly limited to Peyer’s patches (PP). The increase in IL-4-producing cells in ΔdblGATA-1 mice was particularly evident within the CXCR5+PD-1+ T-follicular helper cell population and was associated with a switch of germinal centre B cells to IgG1 production and elevated serum IgG1 levels. In contrast, infected wild-type mice had a modest IgG1 response in the PP, whereas successfully maintaining a population of IgA+ germinal center B cells. Our results suggest a novel role for eosinophils during intestinal infection whereby they restrict IL-4 responses by follicular T helper cells and IgG1 class switching in the PP to ensure maintenance of local IgA production.