ArticleProceedings of the National Academy of Sciences of the United States of America2011
Critical roles of chemokine receptor CCR10 in regulating memory IgA responses in intestines.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
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- A single-cell atlas of intestinal immune cells across the day-night cycle reveals dynamic populations.bioRxiv : the preprint server for biology · 2026Article
- Not all plasma cells are made equal: well-hidden layers of heterogeneity.Frontiers in immunology · 2026Review
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- A Specialized Epithelial Cell Type Regulating Mucosal Immunity and Driving Human Crohn's Disease.bioRxiv : the preprint server for biology · 2023Article
- Selenoprotein W Ameliorates Experimental Colitis and Promotes Intestinal Epithelial Repair.Antioxidants (Basel, Switzerland) · 2023Article
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- Disrupted Peyer's Patch Microanatomy in COVID-19 Including Germinal Centre Atrophy Independent of Local Virus.Frontiers in immunology · 2022Article
- Coordinated co-migration of CCR10Mucosal immunology · 2021Article
- Immunopathology and Immunosenescence, the Immunological Key Words of Severe COVID-19. Is There a Role for Stem Cell Transplantation?Frontiers in cell and developmental biology · 2021Review
- Preferential Perinatal Development of Skin-Homing NK1.1iScience · 2020Article
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- Host Factors Affecting Generation of Immunity Against Porcine Epidemic Diarrhea Virus in Pregnant and Lactating Swine and Passive Protection of Neonates.Pathogens (Basel, Switzerland) · 2020Review
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chemokine receptor CCR10 is expressed by all intestinal IgA-producing plasma cells and is suggested to play an important role in positioning these cells in the lamina propria for proper IgA production to maintain intestinal homeostasis and protect against infection. However, interfering with CCR10 or its ligand did not impair intestinal IgA production under homeostatic conditions or during infection, and the in vivo function of CCR10 in the intestinal IgA response remains unknown. We found that an enhanced generation of IgA(+) cells in isolated lymphoid follicles of intestines offset defective intestinal migration of IgA(+) cells in CCR10-KO mice, resulting in the apparently normal IgA production under homeostatic conditions and in primary response to pathogen infection. However, the compensatorily generated IgA(+) cells in CCR10-KO mice carried fewer hypermutations in their Ig heavy chain alleles than those of WT mice, indicating that their IgA repertoires are qualitatively different, which might impact the intestinal homeostasis of microflora. In addition, CCR10-deficient long-lived IgA-producing plasma cells and IgA(+) memory B cells generated against the pathogen infection could not be maintained properly in intestines. Consequently, IgA memory responses to the pathogen reinfection were severely impaired in CCR10-KO mice. These findings elucidate critical roles of CCR10 in regulating the intestinal IgA response and memory maintenance and could help in design of vaccines against intestinal and possibly other mucosal pathogens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.