Cited by 215T-cell and B-cell ImmunologyReceptor Mechanisms and SignalingPsoriasis: Treatment and Pathogenesis

Mice Lacking the Orphan G Protein-Coupled Receptor G2A Develop a Late-Onset Autoimmune Syndrome

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Le, Lu Q, Kabarowski, Janusz H.S, Weng, Zhigang, Satterthwaite, Anne B, Harvill, Eric T, Jensen, Eric R, Miller, Jeff F, Witte, Owen N·2001·Immunity

Abstract

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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Crossref · 10.1016/s1074-7613(01)00145-5

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  • Autoimmunity is observed in mice whose phagocytes lack G2A, a receptor required for response to lysophosphatidylcholine.

    “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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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
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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