ArticleClinical and experimental immunology1988
Reaction of bacterium-primed murine T cells to cartilage components: a clue for the pathogenesis of arthritis?
Article in Clinical and experimental immunology, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 21 citations in OpenAlex.
- The gut-joint axis in juvenile idiopathic arthritis.Arthritis research & therapy · 2026Review
- Progress does not just come in giant leaps: adapting techniques for the study of inflammation to novel applications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Diversification of T cell responses to carboxy-terminal determinants within the 65-kD heat-shock protein is involved in regulation of autoimmune arthritis.The Journal of experimental medicine · 1997Article
- Prospects of immunotherapy for rheumatoid arthritis.Pharmacy world & science : PWS · 1995Review
- Protection against streptococcal cell wall-induced arthritis by pretreatment with the 65-kD mycobacterial heat shock protein.The Journal of experimental medicine · 1989Article
- The mycobacterial 65 kD heat-shock protein and autoimmune arthritis.Rheumatology international · 1989Review
- Pathogenetic mechanisms in the Mycoplasma arthritidis polyarthritis of rats.Rheumatology international · 1989Review
- Streptococcal cell wall-induced arthritis and flare-up reaction in mice induced by homologous or heterologous cell walls.The American journal of pathology · 1988Article
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
Although different models for rheumatoid arthritis have been studied, the pathogenesis in humans remains unknown. A possible mechanism is the crossreactivity between bacterial components and the target-tissue, the cartilage. The existence of this crossreactivity is supported by various data from clinical and experimental studies. Here we provide direct evidence that priming in vivo with cell wall fragments of Streptococcus pyogenes or Escherichia coli can induce a cellular and humoral anti-cartilage response in Balb/c mice in vitro. T cells isolated from these mice can be stimulated in vitro to proliferate by a variety of antigens among which are the priming bacterium, an unrelated bacterium, small bacterial components and diverse antigens of cartilagenous origin. In bacterium-primed mice antibodies were also detected that displayed a reactivity to cartilage extract besides the reactivity to bacteria. A crossreactive response occurred in vivo in certain circumstances: a delayed type hypersensitivity reaction could be elicited in cell-wall-primed mice by challenge with cartilage extract. For the expression of this crossreactive response in vivo however, it was obligatory to attenuate the mouse's suppressor-circuit. In this paper we would suggest a mechanism for the pathology of chronic arthritis, based on repeated challenges with different bacterial stimuli.
Indexed as
Identifiers
3293852PMC1541500W2401813858What OpenQuestion holds
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.