ArticleJournal of immunology (Baltimore, Md. : 1950)2012
B7x in the periphery abrogates pancreas-specific damage mediated by self-reactive CD8 T cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- B7H4 Role in Solid Cancers: A Review of the Literature.Cancers · 2024Review
- B7-H4 Polymorphism Influences the Prevalence of Diabetes Mellitus and Pro-Atherogenic Dyslipidemia in Patients with Psoriasis.Journal of clinical medicine · 2022Article
- B7 immune-checkpoints as targets for the treatment of neuroendocrine tumors.Endocrine-related cancer · 2021Article
- High lymphocyte‑to‑monocyte ratio is associated with low α‑fetoprotein expression in patients with hepatitis B virus‑associated hepatocellular carcinoma.Molecular medicine reports · 2020Article
- The B7x Immune Checkpoint Pathway: From Discovery to Clinical Trial.Trends in pharmacological sciences · 2019Review
- Extramammary Paget disease shows differential expression of B7 family members B7-H3, B7-H4, PD-L1, PD-L2 and cancer/testis antigens NY-ESO-1 and MAGE-A.Oncotarget · 2019Article
- Donor and host B7-H4 expression negatively regulates acute graft-versus-host disease lethality.JCI insight · 2019Article
- B7x-from bench to bedside.ESMO open · 2019Review
- The expanding repertoire of targets for immune checkpoint inhibition in bladder cancer: What lies beneath the tip of the iceberg, PD-L1.Urologic oncology · 2018Review
- Review and Meta-Analyses of TAAR1 Expression in the Immune System and Cancers.Frontiers in pharmacology · 2018Article
- Tumor-expressed immune checkpoint B7x promotes cancer progression and antigen-specific CD8 T cell exhaustion and suppressive innate immune cells.Oncotarget · 2017Article
- The third group of the B7-CD28 immune checkpoint family: HHLA2, TMIGD2, B7x, and B7-H3.Immunological reviews · 2017Review
- Tumor Regression and Delayed Onset Toxicity Following B7-H4 CAR T Cell Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Loss of Peripheral Protection in Pancreatic Islets by Proteolysis-Driven Impairment of VTCN1 (B7-H4) Presentation Is Associated with the Development of Autoimmune Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- B7x/B7-H4 modulates the adaptive immune response and ameliorates renal injury in antibody-mediated nephritis.Clinical and experimental immunology · 2015Article
- Emerging targets in cancer immunotherapy: beyond CTLA-4 and PD-1.Immunotherapy · 2015Review
- Structure and cancer immunotherapy of the B7 family member B7x.Cell reports · 2014Article
- Nardilysin-dependent proteolysis of cell-associated VTCN1 (B7-H4) marks type 1 diabetes development.Diabetes · 2014Article
- Endocrine autoimmune diseases and female infertility.Nature reviews. Endocrinology · 2014Review
- B7 family checkpoint regulators in immune regulation and disease.Trends in immunology · 2013Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
B7x (B7-H4 or B7S1) is the seventh member of the B7 family, and its in vivo function remains largely unknown. Despite new genetic data linking the B7x gene with autoimmune diseases, how exactly it contributes to peripheral tolerance and autoimmunity is unclear. In this study, we showed that B7x protein was not detected on APCs or T cells in both human and mice, which is unique in the B7 family. Because B7x protein is expressed in some peripheral cells such as pancreatic β cells, we used a CD8 T cell-mediated diabetes model (AI4αβ) in which CD8 T cells recognize an endogenous self-Ag, and found that mice lacking B7x developed more severe diabetes than control AI4αβ mice. Conversely, mice overexpressing B7x in the β cells (Rip-B7xAI4αβ) were diabetes free. Furthermore, adoptive transfer of effector AI4αβ CD8 T cells induced diabetes in control mice, but not in Rip-B7xAI4αβ mice. Mechanistic studies revealed that pathogenic effector CD8 T cells were capable of migrating to the pancreas but failed to robustly destroy tissue when encountering local B7x in Rip-B7xAI4αβ mice. Although AI4αβ CD8 T cells in Rip-B7xAI4αβ and AI4αβ mice showed similar cytotoxic function, cell death, and global gene expression profiles, these cells had greater proliferation in AI4αβ mice than in RIP-B7xAI4αβ mice. These results suggest that B7x in nonlymphoid organs prevents peripheral autoimmunity partially through inhibiting proliferation of tissue-specific CD8 T cells, and that local overexpression of B7x on pancreatic β cells is sufficient to abolish CD8 T cell-induced diabetes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.