Development of Lupus-like Autoimmune Diseases by Disruption of the PD-1 Gene Encoding an ITIM Motif-Carrying Immunoreceptor
Open accessAbstract
PD-1, a 55 kDa transmembrane protein containing an immunoreceptor tyrosine-based inhibitory motif, is induced in lymphocytes and monocytic cells following activation. Aged C57BL/6(B6)-PD-1(-/-) congenic mice spontaneously developed characteristic lupus-like proliferative arthritis and glomerulonephritis with predominant IgG3 deposition, which were markedly accelerated by introduction of a Fas mutation (lpr). Introduction of a PD-1 null mutation into the 2C-TCR (anti-H-2Ld) transgenic mice of the H-2(b/d) background resulted in the chronic and systemic graft-versus-host-like disease. Furthermore, CD8+ 2C-TCR+ PD-1(-/-) T cells exhibited markedly augmented proliferation in vitro in response to H-2d allogenic cells. Collectively, it is suggested that PD-1 is involved in the maintenance of peripheral self-tolerance by serving as a negative regulator of immune responses.
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PD-1 is homologous to CD28, primarily involved in inhibitory immune signaling, and an essential regulator of adaptive immune responses.
“It has since become clear, however, that PD-1, which is homologous to CD28, is primarily involved in inhibitory immune signaling, and is an essential regulator of adaptive immune responses (31).”
From Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018) · cites this paper as [31]
Mice deficient in PD-1 initially appear healthy but develop autoimmune diseases such as lupus-like proliferative glomerulonephritis and arthritis with age and exacerbated inflammation during infections.
“Mice deficient in the receptor initially appear healthy, but develop autoimmune diseases such as lupus-like proliferative glomerulonephritis and arthritis with age and exacerbated inflammation during infections (18, 31, 49, 50).”
From Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018) · cites this paper as [31]
PD-1 knockout mice exhibit lupus-like autoimmune disease with arthritis and cardiomyopathy.
“PD-1 knockouts (Nishimura et al., 1999) and exhibit lupus-like autoimmune disease with arthritis and cardiomyopathy”
From Hallmarks of response, resistance, and toxicity to immune checkpoint blockade (2021) · cites this paper as Nishimura et al., 1999
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- Authors
- Nishimura, H., Nose, M., Hiai, H., Minato, N., & Honjo, T.
- Affiliations
- Kyoto University (JP)
- Ehime University (JP)
- Corresponding author
- Honjo, Tasuku
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 1999-08
- Volume
- 11
- Issue
- 2
- Pages
- 141-151
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2056535502
- Cited by
- 2,749
- References
- 1
- Citations by year
- 2026: 66 · 2025: 85 · 2024: 119 · 2023: 173 · 2022: 152 · 2021: 202 · 2020: 175 · 2019: 192 · 2018: 188 · 2017: 168 · 2016: 137 · 2015: 122 · 2014: 86 · 2013: 81 · 2012: 65
- FWCI
- 18.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- PD-1, ITIM, glomerulonephritis, FAS mutations, lpr mice, graft-versus-host disease, CD8+ T cells, allogeneic T cell proliferation, negative regulation of immune response
- MeSH terms
- Animals, Antigens, Surface, Arthritis, Rheumatoid, H-2 Antigens, Immune Tolerance, Genetic Linkage, Lupus Nephritis, Lymphocyte Activation, Mice, Inbred BALB C, Mice, Transgenic, Proteins, T-Lymphocytes, Mice, Inbred MRL lpr, Apoptosis Regulatory Proteins, Mice, Programmed Cell Death 1 Receptor
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