CD4+ lymphoid tissue inducer cells promote innate immunity in the gut

By Gregory F. Sonnenberg, L. Monticelli, M. Elloso, L. Fouser, D. Artis. Immunity, 2010

611 citations recorded by the source corpus.

SUMMARY Fetal CD4+ lymphoid tissue inducer (LTi) cells play a critical role in the development of lymphoid-tissues. Recent studies identified that LTi cells persist in adults and are related to a heterogeneous population of innate lymphoid cells that have been implicated in inflammatory responses. However, whether LTi cells contribute to protective immunity remains poorly defined. We demonstrate that following infection with Citrobacter rodentium, CD4+ LTi cells were a dominant source of interleukin-22 (IL-22) early during infection. Infection-induced CD4+ LTi cell responses were IL-23-dependent, and ablation of IL-23 impaired innate immunity. Further, depletion of CD4+ LTi cells abrogated infection-induced expression of IL-22 and anti-microbial peptides, resulting in exacerbated host mortality. LTi cells were also found to be essential for host protective immunity in lymphocyte-replete hosts. Collectively these data demonstrate that adult CD4+ LTi cells are a critical source of IL-22 and identify a previously unrecognized function for CD4+ LTi cells in promoting innate immunity in the intestine.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/54a625b04bc9331f2a68367d773b24ee20a64f9b

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In Immunology

1. K. Honda
2. Dan R. Littman
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4. G. Eberl
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6. Liang Zhou
7. A. Jetten
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Citations in the corpus

• Interaction between the gut microbiome and mucosal immune system (2017, background): “22 is produced by ILCs and promotes homeostasis and healing during infection in the gut [28, 29].”
• The Microbiome in Infectious Disease and Inflammation (2012, positive): “rodentium (132), but IL-23-dependent innate lymphoid cells (ILCs) (discussed below) also have key functions (144).”
• The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells (2011, background): “rodentium infection in mice, highlighting the crucial role of RORgt ILCs in innate immune responses (Sonnenberg et al., 2011).”
• RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota (2011, background): “IL-22 has a critical role in defense against attaching and effacing bacterial pathogens in the intestine, such as Citrobacter rodentium”