ArticleInflammatory bowel diseases2012
Role of LFA-1 in the activation and trafficking of T cells: implications in the induction of chronic colitis.
Article in Inflammatory bowel diseases, 2012. 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, 12 citations in OpenAlex.
- The role of integrins in T cell-mediated resistance tobioRxiv : the preprint server for biology · 2026Article
- Recent advances in host-focused molecular tools for investigating host-gut microbiome interactions.Frontiers in microbiology · 2024Review
- LFA-1 knockout inhibited the tumor growth and is correlated with treg cells.Cell communication and signaling : CCS · 2023Article
- The transcription factor Mef2d regulates B:T synapse-dependent GC-TScience immunology · 2023Article
- Review
- β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020Review
- Differential T cell homing to colon vs. small intestine is imprinted by local CD11cJournal of leukocyte biology · 2017Article
- Fine-tuning Tumor Immunity with Integrin Trans-regulation.Cancer immunology research · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
introductionWe have previously demonstrated that adoptive transfer of naïve CD4(+) T cells devoid of lymphocyte function-associated antigen-1-deficient (LFA-1; CD11a/CD18) into recombination activating gene-1 (RAG-1) deficient (RAG(-/-) ) mice fails to induce chronic colitis whereas transfer of wild type (WT) T-cells induces unrelenting and chronic disease.
methodsThe objectives of this study were to assess the role of lymphocyte function-associated antigen-1 (LFA-1) in enteric antigen (EAg)-induced activation of T cells in vitro and in vivo and to define the importance of this integrin in promoting trafficking of T cells to the mesenteric lymph nodes (MLNs) and colon.
resultsWe found that EAg-pulsed dendritic cells (DCs) induced proliferation of LFA-1-deficient (CD11a(-/-) ) CD4(+) T cells that was very similar to that induced using WT T cells, suggesting that LFA-1 is not required for activation/proliferation of T cells in vitro. Coculture of WT or CD11a(-/-) T cells with EAg-pulsed DCs induced the generation of similar amounts of interferon-gamma, interleukin (IL)-4, and IL-10, whereas IL-17A production was reduced ≈ 2-fold in cocultures with CD11a(-/-) T cells. Short-term (20-22 hours) trafficking studies demonstrated that while both WT and CD11a(-/-) T cells migrated equally well into the spleen, liver, lungs, small intestine, cecum, and colon, trafficking of CD11a(-/-) T cells to the MLNs was reduced by 50% when compared to WT T cells. When the observation period was extended to 3-7 days posttransfer, we observed ≈ 2-3-fold more WT T cells within the MLNs and colon than CD11a(-/-) T cells, whereas T-cell proliferation (as measured by CFSE dilution) was comparable in both populations.
conclusionsTaken together, our data suggest that LFA-1 is not required for EAg-induced activation of CD4(+) T cells in vitro or in vivo but is required for trafficking of T cells to the MLNs and homing of colitogenic effector cells to the colon where they initiate chronic gut inflammation.
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