ArticleImmunology1997
Pristane-induced arthritis is CD4+ T-cell dependent.
Article in Immunology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 37 citations in OpenAlex.
- Early Peritoneal CC Chemokine Production Correlates with Divergent Inflammatory Phenotypes and Susceptibility to Experimental Arthritis in Mice.Journal of immunology research · 2019Article
- Mice Selected for Acute Inflammation Present Altered Immune Response during Pristane-Induced Arthritis Progression.BioMed research international · 2018Article
- A modified graft-versus-host-induced model for systemic sclerosis, with pulmonary fibrosis in Rag2-deficient mice.FEBS open bio · 2017Article
- Regulation of Leukocyte Recruitment to the Spleen and Peritoneal Cavity during Pristane-Induced Inflammation.Journal of immunology research · 2017Article
- Characterisation of an epigenetically altered CD4(+) CD28(+) Kir(+) T cell subset in autoimmune rheumatic diseases by multiparameter flow cytometry.Lupus science & medicine · 2016Article
- Pristane-induced arthritis loci interact with the Slc11a1 gene to determine susceptibility in mice selected for high inflammation.PloS one · 2014Article
- Cluster of systemic lupus erythematosus (SLE) associated with an oil field waste site: a cross sectional study.Environmental health : a global access science source · 2007Article
- Slc11a1 (formerly NRAMP1) gene modulates both acute inflammatory reactions and pristane-induced arthritis in mice.Genes and immunity · 2007Article
- Involvement of antibody production quantitative trait loci in the susceptibility to pristane-induced arthritis in the mouse.Genes and immunity · 2006Article
- Complete Freund's adjuvant promotes the increases of IFN-gamma and nitric oxide in suppressing chronic arthritis induced by pristane.Inflammation · 2003Article
- Article
- Role of heat shock proteins in protection from and pathogenesis of infectious diseases.Clinical microbiology reviews · 1999Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of arthritis induced in mice by intraperitoneal injection of the non-antigenic mineral oil pristane (2,6,10,14-tetramethylpentadecane) was shown to depend on the presence of CD4+ T cells. Initial experiments assessed the influx of lymphoid cells into the peritoneal cavity of CBA/Igb mice after pristane injection. Both CD4+ and CD8+ cell numbers were maximal around 50 days. Other experiments confirmed our original observation that irradiated pristane-treated mice failed to develop arthritis unless they were reconstituted with spleen cells from normal donors. This finding has been extended by showing that the population of transferred splenic lymphoid cells must contain CD4+ T cells, while CD8+ T cells and B cells were not required for reconstitution. Conventionally housed and hsp 65-immunized animals are known to harbour T cells reactive with hsp 65. In addition, hsp 65-immunized mice are resistant to the development of pristane-induced arthritis (PIA). Thus, additional experiments assessed the population of splenic T cells activated and proliferating against mycobacterial 65,000 MW heat shock protein (hsp 65). In cultures of purified splenic T cells derived from both conventional and hsp 65-immunized mice, removal of CD4+ T cells significantly reduced the proliferative response to hsp 65, while removal of CD8+ T cells often enhanced the response. These proliferative responses were also shown to be major histocompatibility complex (MHC) class II restricted. The present findings demonstrate that PIA is CD4+ T-cell mediated, and immunodominant environmental antigens such as hsp 65 activate this population of lymphocytes. The CD4+ hsp 65-reactive population may be pathogenic or protective in PIA, depending upon the route of sensitization.
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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.