ArticleThe Journal of experimental medicine2024
Intestinal cDC1s provide cues required for CD4+ T cell-mediated resistance to Cryptosporidium.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Structural Basis for the Immunological Paradox of a High-Affinity Yet Non-Immunogenic MHC-I Epitope fromBiology · 2026Article
- The role of integrins in T cell-mediated resistance tobioRxiv : the preprint server for biology · 2026Article
- Effect of the intestinal microbiota on TSeminars in immunopathology · 2026Review
- De-coupling immune parameters and toxicity associated with IL-12 agonism.Cell reports · 2025Article
- Article
- Article
- Analysis of intestinal epithelial cell responses to Cryptosporidium highlights the temporal effects of IFN-γ on parasite restriction.PLoS pathogens · 2024Article
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11 authors.
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Abstract
Cryptosporidium is an enteric pathogen and a prominent cause of diarrheal disease worldwide. Control of Cryptosporidium requires CD4+ T cells, but how protective CD4+ T cell responses are generated is poorly understood. Here, Cryptosporidium parasites that express MHCII-restricted model antigens were generated to understand the basis for CD4+ T cell priming and effector function. These studies revealed that parasite-specific CD4+ T cells are primed in the draining mesenteric lymph node but differentiate into Th1 cells in the gut to provide local parasite control. Although type 1 conventional dendritic cells (cDC1s) were dispensable for CD4+ T cell priming, they were required for CD4+ T cell gut homing and were a source of IL-12 at the site of infection that promoted local production of IFN-γ. Thus, cDC1s have distinct roles in shaping CD4+ T cell responses to an enteric infection: first, to promote gut homing from the mesLN, and second, to drive effector responses in the intestine.
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