ArticleThe Journal of experimental medicine2005
Deletion of DOCK2, a regulator of the actin cytoskeleton in lymphocytes, suppresses cardiac allograft rejection.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- Association of the Dedicator of Cytokinesis 2 (DOCK2) Gene Polymorphisms with COVID-19 and Plasma LDH, AST, ALT, and Ferritin Levels.Biomolecules · 2026Article
- Interpretable Machine Learning Identifies Hub Biomarkers of Renal Fibrosis and Their Potential Medical Applications.Drug design, development and therapy · 2026Article
- Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease.Signal transduction and targeted therapy · 2025Review
- Single-Cell Transcriptomics Reveals a Pivotal Role of DOCK2 in Sjögren Disease.ACR open rheumatology · 2024Article
- DOCK2 Deficiency Attenuates Abdominal Aortic Aneurysm Formation-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Cancer-derived cholesterol sulfate is a key mediator to prevent tumor infiltration by effector T cells.International immunology · 2022Article
- Insights from DOCK2 in cell function and pathophysiology.Frontiers in molecular biosciences · 2022Review
- SLAMF8 Participates in Acute Renal Transplant RejectionFrontiers in immunology · 2022Article
- The DOCK protein family in vascular development and disease.Angiogenesis · 2021Review
- The role of Dock2 on macrophage migration and functions during Citrobacter rodentium infection.Clinical and experimental immunology · 2021Article
- FLT3-ITD cooperates with Rac1 to modulate the sensitivity of leukemic cells to chemotherapeutic agents via regulation of DNA repair pathways.Haematologica · 2019Article
- Spontaneous Loss-of-FunctionCrohn's & colitis 360 · 2019Article
- The Rac Activator DOCK2 Mediates Plasma Cell Differentiation and IgG Antibody Production.Frontiers in immunology · 2018Article
- DOCK2 interacts with FLT3 and modulates the survival of FLT3-expressing leukemia cells.Leukemia · 2017Article
- Gene Expression in Biopsies of Acute Rejection and Interstitial Fibrosis/Tubular Atrophy Reveals Highly Shared Mechanisms That Correlate With Worse Long-Term Outcomes.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016Article
- Dedicator of cytokinesis 2, a novel regulator for smooth muscle phenotypic modulation and vascular remodeling.Circulation research · 2015Article
- Essential role of Elmo1 in Dock2-dependent lymphocyte migration.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Structural basis for mutual relief of the Rac guanine nucleotide exchange factor DOCK2 and its partner ELMO1 from their autoinhibited forms.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Interplay of polarity proteins and GTPases in T-lymphocyte function.Clinical & developmental immunology · 2012Review
- Immune pathology associated with altered actin cytoskeleton regulation.Autoimmunity · 2010Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allograft rejection is induced by graft tissue infiltration of alloreactive T cells that are activated mainly in secondary lymphoid organs of the host. DOCK2 plays a critical role in lymphocyte homing and immunological synapse formation by regulating the actin cytoskeleton, yet its role in the in vivo immune response remains unknown. We show here that DOCK2 deficiency enables long-term survival of cardiac allografts across a complete mismatch of the major histocompatibility complex molecules. In DOCK2-deficient mice, alloreactivity and allocytotoxicity were suppressed significantly even after in vivo priming with alloantigens, which resulted in reduced intragraft expression of effector molecules, such as interferon-gamma, granzyme B, and perforin. This is mediated, at least in part, by preventing potentially alloreactive T cells from recruiting into secondary lymphoid organs. In addition, we found that DOCK2 is critical for CD28-mediated Rac activation and is required for the full activation of alloreactive T cells. Although DOCK2-deficient, alloreactive T cells were activated in vitro in the presence of exogenous interleukin-2, these T cells, when transferred adoptively, failed to infiltrate into the allografts that were transplanted into RAG1-deficient mice. Thus, DOCK2 deficiency attenuates allograft rejection by simultaneously suppressing multiple and key processes. We propose that DOCK2 could be a novel molecular target for controlling transplant rejection.
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