7/31/2023 0 Comments Antibody repertoire microbiomeWhile it was concluded from each of the above mentioned studies that IgA preferentially binds a taxonomically distinct subset of the whole microbiota, it remains difficult to define a core sIgA-coated community in healthy individuals. ![]() This observation supports earlier studies showing that Lachnospiraceae members are able to elicit innate immune responses and modulate adaptive immune responses in the gut. The relatively high frequency of these organisms in the human colon might account for their prevalence in IgA + fractions. 19, 20 Of note, multiple taxa of the phylum Firmicutes, in particular those belonging to the family Lachnospiraceae, are significantly enriched within the IgA + fraction whatever the human cohort (Table 1). Consistently, most microbes, irrespective of their microbial phylogeny, can induce specific IgA in monocolonized gnotobiotic mice. Second, the four major phyla, namely Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria were detected in IgA-coated microbiota. First, IgA bound a highly diverse fraction of microbiota, including numerous rare genera (generally <1% in frequency). Despite some variations, core features of the IgA-coated subset emerge from these data. 3, 4, 15, 16, 17, 18 Table 1 gathers bacterial taxa that are significantly targeted by IgA in healthy individuals. Several such IgAseq studies have independently described IgA + communities in mice 9, 10, 11, 12, 13, 14 and in humans. 7, 8 Recently, a combination of bacterial flow cytometry with high-throughput 16S gene sequencing offered an opportunity to identify IgA-coated bacteria ex vivo. Here, we review recent murine and human studies in an attempt to provide a comprehensive picture of our current knowledge of the interplay between gut antibodies and microbiota.Įarly studies of gut microbiota revealed that secretory IgA coat only a fraction of human and murine microbiota. However, it has been reported recently that IgG targeting either bacterial antigens, whole bacterial cells, or whole microbial consortia, can also be retrieved from healthy subjects. 5, 6 Finally, systemic IgG responses targeting gut-microbial communities were initially described in IBD and considered merely secondary to bacterial translocations in relation with gut barrier defects. 4 The functional consequences of these observations are unclear, but could be clinically relevant as it is well established that patients selectively lacking IgA rarely develop inflammatory bowel diseases (IBD), which is instead more common and severe in those lacking both IgA and IgM. 3 Moreover, sIgM in healthy humans seem to bind a very restricted fraction of gut microbiota along with secretory IgA. Whereas early studies have shown the presence of IgM plasmocytes in gut biopsies of IgA-deficient patients (IgAd), 1, 2 more recent studies provide evidence that secretory IgM (sIgM) binds a fraction of commensal microbiota in IgA deficiency thereby enhancing bacterial diversity. Novel functions have also been ascribed, albeit putatively, to IgM and IgG at the gut-microbial interface. IgA is now viewed as playing a pivotal role in supporting the establishment, selection, diversification, and long-term maintenance of a healthy commensal gut microbiota. In the past decade, with the advent of microbial metagenomics and the improvement of bacterial flow cytometry, murine and human studies have shed new light on IgA/microbiota commensalism. Notably, the function of secretory Immunoglobulin (Ig) A, given its mucosal localization, has been considered for a long time to be restricted to immune exclusion, i.e., neutralization of luminal pathogens prevention of host invasion. Humoral immunity, in particular antibody-mediated responses, plays a key role in the host defense against extracellular pathogens.
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