ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Lymphopenia-induced proliferation is a potent activator for CD4+ T cell-mediated autoimmune disease in the retina.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Spontaneous organ-specific eye autoimmune disease resulting from two engineered gene mutations compromising immune tolerance.Frontiers in immunology · 2026Review
- Follicular helper- and peripheral helper-like T cells drive autoimmune disease in human immune system mice.eLife · 2025Article
- Parabiosis reveals the correlation between the recruitment of circulating antigen presenting cells to the retina and the induction of spontaneous autoimmune uveoretinitis.Journal of neuroinflammation · 2022Article
- Lymphopenia, Lymphopenia-Induced Proliferation, and Autoimmunity.International journal of molecular sciences · 2021Review
- Treatment With FoxP3+ Antigen-Experienced T Regulatory Cells Arrests Progressive Retinal Damage in a Spontaneous Model of Uveitis.Frontiers in immunology · 2020Article
- Prior to Peripheral Tolerance, Newly Generated CD4 T Cells Maintain Dangerous Autoimmune Potential: Fas- and Perforin-Independent Autoimmunity Controlled by Programmed Death-1.Frontiers in immunology · 2018Article
- Ocular antigen does not cause disease unless presented in the context of inflammation.Scientific reports · 2017Article
- PD-1 Controls Tonic Signaling and Lymphopenia-Induced Proliferation of T Lymphocytes.Frontiers in immunology · 2017Article
- Retinal antigen-specific regulatory T cells protect against spontaneous and induced autoimmunity and require local dendritic cells.Journal of neuroinflammation · 2014Article
- Lymphopenia-induced proliferation in aire-deficient mice helps to explain their autoimmunity and differences from human patients.Frontiers in immunology · 2014Review
- Breakdown of immune privilege and spontaneous autoimmunity in mice expressing a transgenic T cell receptor specific for a retinal autoantigen.Journal of autoimmunity · 2013Article
- Local "on-demand" generation and function of antigen-specific Foxp3+ regulatory T cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Local activation of dendritic cells alters the pathogenesis of autoimmune disease in the retina.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Regulation of CD8(+) T Cell Responses to Retinal Antigen by Local FoxP3(+) Regulatory T Cells.Frontiers in immunology · 2012Article
- Article
- Microbiota innate stimulation is a prerequisite for T cell spontaneous proliferation and induction of experimental colitis.The Journal of experimental medicine · 2010Article
- Peripheral induction of tolerance by retinal antigen expression.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Generation of Regulatory T Cells to Antigen Expressed in the Retina.Current immunology reviewsArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
To study retinal immunity in a defined system, a CD4+ TCR transgenic mouse line (betagalTCR) specific for beta-galactosidase (betagal) was created and used with transgenic mice that expressed betagal in retinal photoreceptor cells (arrbetagal mice). Adoptive transfer of resting betagalTCR T cells, whether naive or Ag-experienced, into arrbetagal mice did not induce retinal autoimmune disease (experimental autoimmune uveoretinitis, EAU) and gave no evidence of Ag recognition. Generation of betagalTCR T cells in arrbetagal mice by use of bone marrow grafts, or double-transgenic mice, also gave no retinal disease or signs of Ag recognition. Arrbetagal mice were also resistant to EAU induction by adoptive transfer of in vitro-activated betagalTCR T cells, even though the T cells were pathogenic if the betagal was expressed elsewhere. In vitro manipulations to increase T cell pathogenicity before transfer did not result in EAU. The only strategy that induced a high frequency of severe EAU was transfer of naive, CD25-depleted, betagalTCR T cells into lymphopenic arrbetagal recipients, implicating regulatory T cells in the T cell inoculum, as well as in the recipients, in the resistance to EAU. Surprisingly, activation of the CD25-depleted betagalTCR T cells before transfer into the lymphopenic recipients reduced EAU. Taken together, the results suggest that endogenous regulatory mechanisms, as well as peripheral induction of regulatory T cells, play a role in the protection from EAU.
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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.