ATP-gated ionotropic P2X7 receptor controls follicular T helper cell numbers in Peyer’s patches to promote host-microbiota mutualism
Open accessAbstract
Microbial colonization of the gut induces the development of gut-associated lymphoid tissue (GALT). The molecular mechanisms that regulate GALT function and result in gut-commensal homeostasis are poorly defined. T follicular helper (Tfh) cells in Peyer's patches (PPs) promote high-affinity IgA responses. Here we found that the ATP-gated ionotropic P2X7 receptor controls Tfh cell numbers in PPs. Lack of P2X7 in Tfh cells enhanced germinal center reactions and high-affinity IgA secretion and binding to commensals. The ensuing depletion of mucosal bacteria resulted in reduced systemic translocation of microbial components, lowering B1 cell stimulation and serum IgM concentrations. Mice lacking P2X7 had increased susceptibility to polymicrobial sepsis, which was rescued by Tfh cell depletion or administration of purified IgM. Thus, regulation of Tfh cells by P2X7 activity is important for mucosal colonization, which in turn results in IgM serum concentrations necessary to protect the host from bacteremia.
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The subsequent reduction in B1-cell stimulation is believed to cause increased susceptibility of P2rx7−/− mice to polymicrobial sepsis.
“The subsequent reduction in B1-cell stimulation is believed to cause increased susceptibility of P2rx7−/− mice to polymicrobial sepsis (Proietti et al., 2014).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Proietti et al., 2014
This results in an increase in high-affinity IgA specific for intestinal bacteria secreted into the lumen and a depletion of the gut microbiota.
“This results in an increase in high-affinity IgA specific for intestinal bacteria secreted into the intestinal lumen and thereby a depletion of the gut microbiota.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Proietti et al., 2014
P2rx7−/− mice have elevated Tfh cell numbers in the intestinal mucosa, presumably because they are resistant to ATP-induced cell death.
“Mice deficient for P2X7 (P2rx7−/−) have elevated Tfh cell numbers in the intestinal mucosa, presumably because they are resistant to ATP-induced cell death.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Proietti et al., 2014
Impairment of Tfh cells resulting from lack of expression of PD-1 or P2RX7 can alter gut microbiota composition.
“Tfh cells are implicated in maintenance of microbiota homeostasis as highlighted by studies showing that impairment of Tfh cells resulting from lack of expression of co-receptor programmed cell death 1 (PD-1) or ATP-gated ionotropic P2RX7 receptor can alter gut microbiota composition.117,118”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [118]
Sensing of commensal-derived lipopolysaccharide is necessary for development of B1 cells in mouse spleen and for maintenance of basal circulating IgM, which protects in the cecal ligation and puncture sepsis model.
“sensing of commensal-derived LPS has been shown to be necessary for the development of B1 cells in mouse spleen and for the maintenance of basal levels of circulating IgM, which exert a protective role in the cecal ligation and puncture (CLP)-induced sepsis model [47].”
From Antibiotic-Induced Changes in the Intestinal Microbiota and Disease (2016) · cites this paper as [47]
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- Authors
- Proietti, M., Cornacchione, V., Rezzonico Jost, T., Romagnani, A., Faliti, C. E., Perruzza, L., Rigoni, R., Radaelli, E., Caprioli, F., Preziuso, S., Brannetti, B., Thelen, M., McCoy, K. D., Slack, E., Traggiai, E., & Grassi, F.
- Affiliations
- Institute for Research in Biomedicine (CH)
- Novartis (Switzerland) (CH)
- University of Bern (CH)
- Fondazione Filarete (IT)
- University of Milan (IT)
- Università di Camerino (IT)
- ETH Zurich (CH)
- Corresponding author
- Grassi, Fabio
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 41
- Issue
- 5
- Pages
- 789-801
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1996252358
- Cited by
- 181
- References
- 65
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 14 · 2023: 16 · 2022: 21 · 2021: 22 · 2020: 24 · 2019: 26 · 2018: 12 · 2017: 14 · 2016: 11 · 2015: 5
- FWCI
- 7.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- BORIS (University Library Bern) (submittedVersion)
- Unicam Scientific Publications (University of Camerino) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- P2X7 receptor, T follicular helper cells, Peyer's patches, gut-associated lymphoid tissue, IgA, germinal center, mucosal colonization, IgM, polymicrobial sepsis, bacteremia, B-1 cells, commensal bacteria
- MeSH terms
- Adenosine Triphosphate, Animals, B-Lymphocytes, T-Lymphocytes, Helper-Inducer, Humans, Immunoglobulin A, Immunoglobulin M, Intestinal Mucosa, Lymphocyte Depletion, Mice, Inbred C57BL, Peyer's Patches, Symbiosis, Bacteremia, Mice, Knockout, Sepsis, Germinal Center, Genetic Predisposition to Disease, Mice, Receptors, Purinergic P2X7, Microbiota
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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