ArticleClinical and experimental immunology2002
B7-1 and B7-2 co-stimulatory molecules are required for mercury-induced autoimmunity.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 30 citations in OpenAlex.
- Mercury-induced inflammation and autoimmunity.Biochimica et biophysica acta. General subjects · 2019Review
- Invariant Natural Killer T Cells Promote T Cell Immunity by Modulating the Function of Lung Dendritic Cells during Chlamydia pneumoniae Infection.Journal of innate immunity · 2015Article
- Low-dose mercury heightens early innate response to coxsackievirus infection in female mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- The role of decay accelerating factor in environmentally induced and idiopathic systemic autoimmune disease.Autoimmune diseases · 2014Review
- Article
- Spontaneous allograft tolerance in B7-deficient mice independent of preexisting endogenous CD4+CD25+ regulatory T-cells.Transplantation · 2007Article
- Bacterial lipopolysaccharide both renders resistant mice susceptible to mercury-induced autoimmunity and exacerbates such autoimmunity in susceptible mice.Clinical and experimental immunology · 2005Article
- Role of B7 costimulatory molecules in immune responses and T-helper cell differentiation in response to recombinant HagB from Porphyromonas gingivalis.Infection and immunity · 2004Article
- Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus.Environmental health perspectives · 2003Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
B7-1 (CD80) and B7-2 (CD86) molecules on antigen presenting cells play important roles in providing co-stimulatory signals required for activation and expansion of autoreactive T cells. Moreover, some reports have suggested that these molecules may have distinct functions in the differentiation of Th1 and Th2 cells. Mercury-induced autoimmunity in H-2s mice is characterized by lymphoproliferation of T and B cells, serum increases in IgG1 and IgE and production of antinucleolar antibodies (ANoA). The mechanisms responsible for the various manifestations of this syndrome have yet to be elucidated. To examine the contributions of B7 co-stimulatory molecules to this model, susceptible mice were treated with antibodies to B7-1, B7-2, or both during the development of mercury-induced autoimmunity. The combination of anti-B7-1 and anti-B7-2 antibodies prevented Hg-induced disease in H-2s mice. Additionally, single anti-B7-1 antibody treatment was sufficient to prevent Hg-induced ANoA production, but not IgG1 and IgE hypergammaglobulinaemia. Further, single antibody treatment with anti-B7-2 resulted in a partial reduction of ANoA titres but had no significant effect on total serum IgG1 and IgE levels. Taken together, these results indicate that B7-1 and B7-2 molecules are critical for the development of Hg-induced autoimmunity and suggest that the different manifestations of the syndrome are regulated by independent mechanisms.
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