The DOI matches its Crossref record; 49 of the 50 references it cites were found in a registry or an index.
Mice Lacking the Orphan G Protein-Coupled Receptor G2A Develop a Late-Onset Autoimmune Syndrome
Open accessAbstract
Mice with a targeted disruption of the gene encoding a lymphoid-expressed orphan G protein-coupled receptor, G2A, demonstrate a normal pattern of T and B lineage differentiation through young adulthood. As G2A-deficient animals age, they develop secondary lymphoid organ enlargement associated with abnormal expansion of both T and B lymphocytes. Older G2A-deficient mice (>1 year) develop a slowly progressive wasting syndrome, characterized by lymphocytic infiltration into various tissues, glomerular immune complex deposition, and anti-nuclear autoantibodies. G2A-deficient T cells are hyperresponsive to TCR stimulation, exhibiting enhanced proliferation and a lower threshold for activation. Our findings demonstrate that G2A plays a critical role in controlling peripheral lymphocyte homeostasis and that its ablation results in the development of a novel, late-onset autoimmune syndrome.
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“However, autoimmunity has been observed in mice in which phagocytes lack the G-protein coupled receptor G2A41, which is required for the response to lysophosphatidylcholine 42”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [42]
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Negative regulation of lymphocyte activation and autoimmunity by the molecular adaptor Cbl-b
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Cbl-b regulates the CD28 dependence of T-cell activation
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Metadata
- Authors
- Le, L. Q., Kabarowski, J. H. S., Weng, Z., Satterthwaite, A. B., Harvill, E. T., Jensen, E. R., Miller, J. F., & Witte, O. N.
- Affiliations
- University of California, Los Angeles (US)
- The University of Texas Southwestern Medical Center (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Witte, Owen N
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2001-05
- Volume
- 14
- Issue
- 5
- Pages
- 561-571
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2095533402
- Cited by
- 215
- References
- 50
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 6 · 2023: 3 · 2022: 4 · 2021: 7 · 2020: 10 · 2019: 9 · 2018: 8 · 2017: 9 · 2016: 6 · 2015: 4 · 2014: 4 · 2013: 3 · 2012: 7
- FWCI
- 5.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca076204-05)
- National Cancer Institute (CA76204, T32 CA090576)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- G2A, orphan G protein-coupled receptor, knockout mice, lymphocyte homeostasis, B cell hyperactivation, cachexia, immune complex deposition, antinuclear antibodies, aging
- MeSH terms
- Animals, Autoimmune Diseases, B-Lymphocytes, Cell Division, Female, Lymph Nodes, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Receptors, Antigen, T-Cell, Receptors, Cell Surface, T-Lymphocytes, Time Factors, Autoimmunity, Mice, Knockout, Cell Cycle Proteins, GTP-Binding Proteins, Receptors, G-Protein-Coupled, Mice
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