ArticleMolecular immunology2008
Requirement of Galphai in thymic homing and early T cell development.
Article in Molecular immunology, 2008. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- MAGIS syndrome: phenotypes, pathogenesis, and treatment.Journal of human immunity · 2025Article
- Loss of GαScientific reports · 2017Article
- The impact of RGS and other G-protein regulatory proteins on Gαi-mediated signaling in immunity.Biochemical pharmacology · 2016Review
- Implications of non-canonical G-protein signaling for the immune system.Cellular signalling · 2014Review
- A quantitative study of the mechanisms behind thymic atrophy in Gαi2-deficient mice during colitis development.PloS one · 2012Article
- FTY720 blocks egress of T cells in part by abrogation of their adhesion on the lymph node sinus.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Variations in Gnai2 and Rgs1 expression affect chemokine receptor signaling and the organization of secondary lymphoid organs.Genes and immunity · 2010Article
- Magnetic resonance imaging of radiation-induced thymic atrophy as a model for pathologic changes in acute feline immunodeficiency virus infection.Journal of feline medicine and surgery · 2009Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Demonstration of thymic homing dependent on Galphai proteins is one of the keys to determine whether thymic entrance of blood-borne progenitors is a highly selective process. The present study provides compelling evidence of an indispensable role for Galphai proteins in this process. Absence of either Galphai2 or Galphai3 significantly abrogated thymic homing, with an effect of Galphai3 being greater than that of Galphai2. Pertussis toxin treatment that blocks both Galphai2 and Galphai3 almost completely blocked thymic seeding in the thymus. Null mutation of Galphai3 also hindered bone marrow cell development and thus reduced production of pre-thymic progenitors. In contrast, Galphai2 exhibited a more prominent role than Galphai3 in guidance of CD4-CD8--double negative (DN) 1 cell migration and early thymic differentiation. The Galphai-deficiency-induced defects might be compensated for in part via augmented function of thymic stromal cells so that a nearly normal output of mature T cells could be maintained in these Galphai-deficient mice. These studies underscore the importance of Galphai in regulating thymic homing and pre-thymic and early thymocyte differentiation.
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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.