Expression of the PD-1 antigen on the surface of stimulated mouse T and B lymphocytes
Abstract
A mAb J43 has been produced against the product of the mouse PD-1 gene, a member of the Ig gene superfamily, which was previously isolated from an apoptosis-induced T cell hybridoma (2B4.11) by using subtractive hybridization. Analyses by flow cytometry and immunoprecipitation using the J43 mAb revealed that the PD-1 gene product is a 50-55 kDa membrane protein expressed on the cell surface of several PD-1 cDNA transfectants and 2B4.11 cells. Since the molecular weight calculated from the amino acid sequence is 29, 310, the PD-1 protein appears to be heavily glycosylated. Normal murine lymphoid tissues such as thymus, spleen, lymph node and bone marrow contained very small numbers of PD-1(+) cells. However, a significant PD-1(+) population appeared in the thymocytes as well as T cells in spleen and lymph nodes by the in vivo anti-CD3 mAb treatment. Furthermore, the PD-1 antigen expression was strongly induced in distinct subsets of thymocytes and spleen T cells by in vitro stimulation with either anti-CD3 mAb or concanavalin A (Con A) which could lead T cells to both activation and cell death. Similarly, PD-1 expression was induced on spleen B cells by in vitro stimulation with anti-IgM antibody. By contrast, PD-1 was not significantly expressed on lymphocytes by treatment with growth factor deprivation, dexamethasone or lipopolysaccharide. These results suggest that the expression of the PD-1 antigen is tightly regulated and induced by signal transduction through the antigen receptor and do not exclude the possibility that the PD-1 antigen may play a role in clonal selection of lymphocytes although PD-1 expression is not required for the common pathway of apoptosis.
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Most circulating T cells do not express PD-1 but can be induced to do so upon stimulation through the TCR complex or cytokines such as IL-2, IL-7, IL-15, IL-21, and TGF-β.
“Although most circulating T cells do not express the receptor, they can be induced to do so upon stimulation, through the T cell receptor (TCR) complex or exposure to cytokines such as IL-2, IL-7, IL-15, IL-21, and transforming growth factor (TGF)-β (33, 34).”
From Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018) · cites this paper as [33]
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- Authors
- Agata, Y., Kawasaki, A., Nishimura, H., Ishida, Y., Tsubat, T., Yagita, H., & Honjo, T.
- Affiliations
- Kyoto University (JP)
- Juntendo University (JP)
- Venue
- International Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1996
- Volume
- 8
- Issue
- 5
- Pages
- 765-772
- ISSN
- 0953-8178 (ISSN-L)
- 1460-2377
- OpenAlex
- W2145871366
- Cited by
- 1,589
- References
- 1
- Citations by year
- 2026: 44 · 2025: 71 · 2024: 82 · 2023: 99 · 2022: 107 · 2021: 139 · 2020: 111 · 2019: 107 · 2018: 98 · 2017: 102 · 2016: 79 · 2015: 59 · 2014: 50 · 2013: 49 · 2012: 42
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- PD-1, T cells, B cells, thymocytes, anti-CD3 stimulation, concanavalin A, anti-IgM stimulation, apoptosis, glycosylation, clonal selection, antigen receptor signaling
- MeSH terms
- Animals, Antibodies, Monoclonal, Antigens, Surface, B-Lymphocytes, Cell Line, Cricetulus, Female, Flow Cytometry, Cricetinae, Lymphocyte Activation, Mice, Inbred C57BL, Neoplasm Proteins, Precipitin Tests, Proteins, T-Lymphocytes, Apoptosis Regulatory Proteins, Mice, Programmed Cell Death 1 Receptor
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