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Details

Autor(en) / Beteiligte
Titel
Innate and Adaptive Humoral Responses Coat Distinct Commensal Bacteria with Immunoglobulin A
Ist Teil von
  • Immunity (Cambridge, Mass.), 2015-09, Vol.43 (3), p.541-553
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2015
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • Immunoglobulin A (IgA) is prominently secreted at mucosal surfaces and coats a fraction of the intestinal microbiota. However, the commensal bacteria bound by IgA are poorly characterized and the type of humoral immunity they elicit remains elusive. We used bacterial flow cytometry coupled with 16S rRNA gene sequencing (IgA-Seq) in murine models of immunodeficiency to identify IgA-bound bacteria and elucidate mechanisms of commensal IgA targeting. We found that residence in the small intestine, rather than bacterial identity, dictated induction of specific IgA. Most commensals elicited strong T-independent (TI) responses that originated from the orphan B1b lineage and from B2 cells, but excluded natural antibacterial B1a specificities. Atypical commensals including segmented filamentous bacteria and Mucispirillum evaded TI responses but elicited T-dependent IgA. These data demonstrate exquisite targeting of distinct commensal bacteria by multiple layers of humoral immunity and reveal a specialized function of the B1b lineage in TI mucosal IgA responses. [Display omitted] •IgA predominantly targets commensal bacteria that reside in the small intestine•Most commensal bacteria elicit strong T-independent IgA responses•A minor subset of bacteria evade T-independent IgA and elicit T-dependent responses•The orphan B1b lineage is a prominent source of commensal-specific IgA Bendelac and colleagues find that homeostatic IgA responses target commensal bacteria that reside in the small intestine but exclude bacteria indigenous to the colon. Most commensals are targeted by T-independent IgA derived predominantly from the orphan B1b lineage, but atypical subsets evade T-independent responses and elicit T-dependent IgA.

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