Segmented filamentous bacterium uses secondary and tertiary lymphoid tissues to induce gut IgA and specific T helper 17 cell responses

Emelyne Lécuyer, Sabine Rakotobe, Hélène Lengliné-Garnier, Corinne Lebreton, Marion Picard, Catherine Juste, Rémi Fritzen, Gérard Eberl, Kathy D McCoy, Andrew J Macpherson, Claude-Agnès Reynaud, Nadine Cerf-Bensussan, Valérie Gaboriau-Routhiau

Research output: Contribution to journalArticlepeer-review

197 Citations (Scopus)


Segmented filamentous bacterium (SFB) is a symbiont that drives postnatal maturation of gut adaptive immune responses. In contrast to nonpathogenic E. coli, SFB stimulated vigorous development of Peyer's patches germinal centers but paradoxically induced only a low frequency of specific immunoglobulin A (IgA)-secreting cells with delayed accumulation of somatic mutations. Moreover, blocking Peyer's patch development abolished IgA responses to E. coli, but not to SFB. Indeed, SFB stimulated the postnatal development of isolated lymphoid follicles and tertiary lymphoid tissue, which substituted for Peyer's patches as inductive sites for intestinal IgA and SFB-specific T helper 17 (Th17) cell responses. Strikingly, in mice depleted of gut organized lymphoid tissue, SFB still induced a substantial but nonspecific intestinal Th17 cell response. These results demonstrate that SFB has the remarkable capacity to induce and stimulate multiple types of intestinal lymphoid tissues that cooperate to generate potent IgA and Th17 cell responses displaying only limited target specificity.

Original languageEnglish
Pages (from-to)608-20
Number of pages13
JournalGenes and Immunity
Issue number4
Publication statusPublished - 17 Apr 2014


  • Animals
  • Antigens, Bacterial
  • Cell Communication
  • Cell Differentiation
  • Clostridium
  • Clostridium Infections
  • Escherichia coli
  • Escherichia coli Infections
  • Host-Pathogen Interactions
  • Immunoglobulin A
  • Intestines
  • Lymphoid Tissue
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Peyer's Patches
  • Plasma Cells
  • Th17 Cells
  • Journal Article
  • Research Support, Non-U.S. Gov't


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