ArticlePloS one2009
CD152 (CTLA-4) determines CD4 T cell migration in vitro and in vivo.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Selecting the optimal cell migration assay: fundamentals and practical guidelines.Nature methods · 2026Review
- Association of Cytotoxic T-Lymphocyte Antigen-4 (International journal of molecular sciences · 2024Article
- Increased extracellular vesicles (EVs) related to T cell-mediated inflammation and vascular function in familial hypercholesterolemia.Atherosclerosis plus · 2023Article
- Review
- Pulmonary endothelium-derived PD-L1 induced by the H9N2 avian influenza virus inhibits the immune response of T cells.Virology journal · 2020Article
- Biomarkers of immune checkpoint inhibitor efficacy in cancer.Current oncology (Toronto, Ont.) · 2020Review
- CTLA-4 and PD-1 Control of T-Cell Motility and Migration: Implications for Tumor Immunotherapy.Frontiers in immunology · 2018Review
- Accessory proteins for heterotrimeric G-proteins in the kidney.Frontiers in physiology · 2015Review
- Rab8 binding to immune cell-specific adaptor LAX facilitates formation of trans-Golgi network-proximal CTLA-4 vesicles for surface expression.Molecular and cellular biology · 2014Article
- Diverse mechanisms regulate the surface expression of immunotherapeutic target ctla-4.Frontiers in immunology · 2014Review
- High-sensitivity immunofluorescence staining: a comparison of the liposome procedure and the FASER technique on mGR detection.Journal of fluorescence · 2013Article
- Article
- Migration of Th1 lymphocytes is regulated by CD152 (CTLA-4)-mediated signaling via PI3 kinase-dependent Akt activation.PloS one · 2012Article
- CTLA4 is expressed on mature dendritic cells derived from human monocytes and influences their maturation and antigen presentation.BMC immunology · 2011Article
- Inflammation and epstein-barr virus infection are common features of myasthenia gravis thymus: possible roles in pathogenesis.Autoimmune diseases · 2011Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMigration of antigen-experienced T cells to secondary lymphoid organs and the site of antigenic-challenge is a mandatory prerequisite for the precise functioning of adaptive immune responses. The surface molecule CD152 (CTLA-4) is mostly considered as a negative regulator of T cell activation during immune responses. It is currently unknown whether CD152 can also influence chemokine-driven T cell migration. METHODOLOGY/PRINCIPAL
findingsWe analyzed the consequences of CD152 signaling on Th cell migration using chemotaxis assays in vitro and radioactive cell tracking in vivo. We show here that the genetic and serological inactivation of CD152 in Th1 cells reduced migration towards CCL4, CXCL12 and CCL19, but not CXCL9, in a G-protein dependent manner. In addition, retroviral transduction of CD152 cDNA into CD152 negative cells restored Th1 cell migration. Crosslinking of CD152 together with CD3 and CD28 stimulation on activated Th1 cells increased expression of the chemokine receptors CCR5 and CCR7, which in turn enhanced cell migration. Using sensitive liposome technology, we show that mature dendritic cells but not activated B cells were potent at inducing surface CD152 expression and the CD152-mediated migration-enhancing signals. Importantly, migration of CD152 positive Th1 lymphocytes in in vivo experiments increased more than 200% as compared to CD152 negative counterparts showing that indeed CD152 orchestrates specific migration of selected Th1 cells to sites of inflammation and antigenic challenge in vivo. CONCLUSIONS/SIGNIFICANCE: We show here, that CD152 signaling does not just silence cells, but selects individual ones for migration. This novel activity of CD152 adds to the already significant role of CD152 in controlling peripheral immune responses by allowing T cells to localize correctly during infection. It also suggests that interference with CD152 signaling provides a tool for altering the cellular composition at sites of inflammation and antigenic challenge.
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Registered trials
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.