ArticleAmerican journal of respiratory cell and molecular biology2011
Inducible costimulator controls migration of T cells to the lungs via down-regulation of CCR7 and CD62L.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Metabolic priming of GD2Molecular therapy. Methods & clinical development · 2024Article
- Engagement of the costimulatory molecule ICOS in tissues promotes establishment of CD8Immunity · 2022Article
- Inducible Costimulator-C-X-C Motif Chemokine Receptor 3 Signaling is Involved in Chronic Obstructive Pulmonary Disease Pathogenesis.International journal of chronic obstructive pulmonary disease · 2022Article
- ICOSFrontiers in immunology · 2020Review
- ICOS protects against mortality from acute lung injury through activation of IL-5Mucosal immunology · 2018Article
- Down-Regulation of CD62L Shedding in T Cells by CD39The Journal of investigative dermatology · 2017Article
- Retrogenic ICOS Expression Increases Differentiation of KLRG-1hiCD127loCD8+ T Cells during Listeria Infection and Diminishes Recall Responses.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Effector and central memory T helper 2 cells respond differently to peptide immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Location, location, location: the impact of migratory heterogeneity on T cell function.Frontiers in immunology · 2013Review
- ICOS-expressing lymphocytes promote resolution of CD8-mediated lung injury in a mouse model of lung rejection.PloS one · 2013Article
- ICOS regulates the generation and function of human CD4+ Treg in a CTLA-4 dependent manner.PloS one · 2013Article
- Regulatory T cells and the control of the allergic response.Journal of allergy · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We and others reported that inducible costimulator-deficient (ICOS(-/-)) mice manifest a defect in Th2-mediated airway inflammation, which was attributed to reduced Th2 differentiation in the absence of ICOS signaling. Interestingly, the number of CD4 T cells present in the airways and lungs after sensitization and challenge is significantly reduced in ICOS(-/-) mice. We now show that this reduction is not attributable simply to a reduced proliferation of ICOS(-/-) cells, because significantly more ICOS(-/-) than wild-type activated CD4 T cells are present in the lymph nodes, suggesting that more ICOS(-/-) CD4 T cells than wild-type CD4 T cells migrated into the lymph nodes. Further investigation revealed that activated ICOS(-/-) CD4 T cells express higher concentrations of the lymph node homing receptors, CCR7 and CD62L, than do wild-type CD4 T cells, leading to a preferential return of ICOS(-/-) cells to the nondraining lymph nodes rather than the lungs. Blocking reentry into the lymph nodes after the initiation of Th2-mediated airway inflammation equalized the levels of CD4 and granulocyte infiltration in the lungs of wild-type and ICOS(-/-) mice. Our results demonstrate that in wild-type CD4 T cells, co-stimulation with ICOS promotes the down-regulation of CCR7 and CD62L after activation, leading to a reduced return of activated CD4 T cells to the lymph nodes and a more efficient entry into the lungs.
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