CD80 (B7) and CD86 (B70) provide similar costimulatory signals for T cell proliferation, cytokine production, and generation of CTL.
Abstract
Signals initiated through both the TCR complex and CD28 are required for optimal activation of T lymphocytes. Recently, it has been demonstrated that CD28 interacts with two different ligands, designated CD80 (B7/B7-1) and CD86 (B70/B7-2). We have produced stable transfectants that express CD80, CD86, or both ligands and have examined their ability to costimulate T cell proliferation, cytokine production, and the generation of CTL. When we used small, resting human peripheral blood T cells as responders, both CD80 and CD86 transfectants efficiently costimulated anti-CD3 mAb-induced proliferation and the secretion of IL-2 and IFN-gamma. Additionally, both CD80 and CD86 transfectants were able to generate functional CTL. The magnitude and kinetics of these responses were similar, which indicates that both ligands provide efficient costimulatory signals. Because many APCs coexpress both CD80 and CD86, we compared the ability of anti-CD80 and anti-CD86 mAbs to inhibit allogeneic MLR stimulated with B lymphoblastoid cell lines and showed that it is necessary to inhibit interactions with both ligands to optimally block CD28-dependent proliferation. Given the limited homology of CD80 and CD86, it was surprising that the binding of CD28-Ig fusion protein to CD80 and that to CD86 transfectants were essentially indistinguishable. Binding of CTLA-4-Ig fusion protein to both transfectants also was quite similar, but was of higher affinity than CD28-Ig binding. Results from these studies…
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CD80 and CD86 are traditionally expressed by antigen-presenting cells and bind CD28 and CTLA-4 on T cells.
“CD80 and CD86 are traditionally expressed by antigen-presenting cells and bind CD28 and CTLA-4 on T cells.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [42]
CD80 and CD86 are potent T-cell co-stimulators, and CD28 tunes the quality, duration, and metabolic consequences of immune activation.
“Early studies in the 1990s established CD80 and CD86 as potent T-cell co-stimulators, while later reviews refined the view of CD28 as a receptor that does not simply “turn on” T cells, but tunes the quality, duration, and metabolic consequences of immune activation [40,41,42].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [42]
In Alzheimer's disease and aging, microglia and peripheral myeloid cells may express co-stimulatory ligands, but the ligand-receptor architecture within the plaque microenvironment remains incompletely defined.
“In Alzheimer’s disease and aging, microglia and peripheral myeloid cells may express co-stimulatory ligands, but the ligand–receptor architecture within the plaque microenvironment remains incompletely defined.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [42]
CD28 is a co-stimulatory receptor on T cells; engagement by CD80 and CD86 on antigen-presenting cells provides a second signal supporting T-cell activation, survival, proliferation, cytokine production, and differentiation.
“In classical immunology, CD28 is best known as a co-stimulatory receptor on T cells. Its engagement by the B7-family ligands CD80 and CD86 on antigen-presenting cells provides a second signal that supports T-cell activation, survival, proliferation, cytokine production, and differentiation.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [42]
Without CD28 co-stimulation, antigen recognition alone may lead to incomplete activation, tolerance, or anergy.
“Without this co-stimulatory context, antigen recognition alone may lead to incomplete activation, tolerance, or anergy.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [42]
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Cited by 480
- Authors
- Lanier, L. L., O'Fallon, S., Somoza, C., Phillips, J. H., Linsley, P. S., Okumura, K., Ito, D., & Azuma, M.
- Affiliations
- Department of Human Immunology, DNAX Research Institute of Molecular and Cellular Biology, Inc. , Palo Alto, CA 94304
- Bristol-Myers Squibb (United States) (US)
- Juntendo University (JP)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1995-01-01
- Volume
- 154
- Issue
- 1
- Pages
- 97-105
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1509098294
- Cited by
- 480
- References
- 0
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 10 · 2023: 8 · 2022: 10 · 2021: 13 · 2020: 13 · 2019: 13 · 2018: 8 · 2017: 10 · 2016: 4 · 2015: 1 · 2014: 16 · 2013: 5 · 2012: 6
- FWCI
- 19.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- CD80, CD86, costimulation, T cell activation, CD28, CTLA-4, T cell proliferation, cytokine production, cytotoxic T lymphocytes, antigen-presenting cells, allogeneic mixed lymphocyte reaction, interleukin-2, interferon-gamma
- MeSH terms
- Adult, Animals, Cell Line, Transformed, Chlorocebus aethiops, Gene Expression Regulation, Humans, L Cells, Lymphocyte Culture Test, Mixed, Ligands, Lymphocyte Activation, Membrane Glycoproteins, Mast-Cell Sarcoma, T-Lymphocytes, Cytotoxic, Tumor Cells, Cultured, Signal Transduction, Antigens, CD, Cytokines, CD28 Antigens, B7-1 Antigen, Mice, B7-2 Antigen
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