ArticleThe Journal of experimental medicine1993
Regulatory role of OX22high T cells in mercury-induced autoimmunity in the brown Norway rat.
Article in The Journal of experimental medicine, 1993. 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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Who cites it
18 citing papers in PubMed.
- Characterization of Rat ILCs Reveals ILC2 as the Dominant Intestinal Subset.Frontiers in immunology · 2020Article
- Genetic control of HgCl2-induced IgE and autoimmunity by a 117-kb interval on rat chromosome 9 through CD4 CD45RChigh T cells.Genes and immunity · 2013Article
- Article
- Influence of PMN leukocyte-mediated pancreatic damage on the systemic immune response in severe acute pancreatitis in rats.Digestive diseases and sciences · 2004Article
- A central role for the mast cell in early phase vasculitis in the Brown Norway rat model of vasculitis: a histological study.International journal of experimental pathology · 2004Article
- Lack of graft-versus-host-like pathology in mercury-induced autoimmunity of Brown Norway rats.Clinical immunology (Orlando, Fla.) · 2003Article
- Exogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat.Clinical and experimental immunology · 2000Article
- Early vasculitis in the mercuric chloride induced Brown Norway rat model is neutrophil independent.International journal of experimental pathology · 1999Article
- Murine mercury-induced autoimmunity: a model of chemically related autoimmunity in humans.Immunologic research · 1999Review
- Mercury-induced autoimmunity in the absence of IL-4.Clinical and experimental immunology · 1998Article
- Transforming growth factor beta (TGF-beta)-dependent inhibition of T helper cell 2 (Th2)-induced autoimmunity by self-major histocompatibility complex (MHC) class II-specific, regulatory CD4(+) T cell lines.The Journal of experimental medicine · 1997Article
- Role of neutrophils in the pathogenesis of experimental vasculitis.The American journal of pathology · 1996Article
- Mercury: god of Th2 cells?Clinical and experimental immunology · 1995Review
- Mercuric chloride, a chemical responsible for T helper cell (Th)2-mediated autoimmunity in brown Norway rats, directly triggers T cells to produce interleukin-4.The Journal of clinical investigation · 1995Article
- T cells reactive to an inducible heat shock protein induce disease in toxin-induced interstitial nephritis.The Journal of experimental medicine · 1994Article
- Use of methyl prednisolone and antioxidants in mercuric chloride-induced experimental vasculitis.Clinical and experimental immunology · 1994Article
- Effects of decomplementation with cobra venom factor on experimental vasculitis.Clinical and experimental immunology · 1994Article
- T cell subsets in glomerular diseases.Springer seminars in immunopathology · 1994Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monoclonal antibody OX22 defines a functional split within CD4+ T cells in the rat, with OX22high cells mainly producing interleukin 2 (IL-2) and interferon gamma and responsible for delayed-type hypersensitivity responses, and OX22low cells mainly producing IL-4 and -5 and responsible for providing B cell help. There are reciprocal interactions between OX22high and OX22low cells, and it has been suggested that the OX22low subset has a role in the prevention of autoimmunity. We have used OX22 in vivo to define the role of these subsets in mercuric chloride-induced autoimmunity in the Brown Norway rat. In this model, there is polyclonal B cell activation and animals develop widespread tissue injury. Treatment of thymectomized animals with OX22 led to a profound reduction in the number of OX22high T cells in the peripheral blood. OX22-treated animals consistently developed more severe tissue injury than controls given an irrelevant antibody of the same isotype. Control animals pretreated with broad spectrum antimicrobial drugs showed milder tissue injury, but this protective effect of antimicrobials was lost in OX22-treated animals. Transfer of naive T cells to OX22-treated animals provided protection, but if T cells were depleted in vitro of OX22high cells before transfer, this effect was lost. These data provide evidence for a protective immunoregulatory role for OX22high T cells in mercuric chloride-induced autoimmunity.
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