ArticleRheumatology (Oxford, England)2022
Recombinant CD300c-Ig fusion protein attenuates collagen-induced arthritis in mice.
Article in Rheumatology (Oxford, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Defining the marker and developmental trajectory of myeloid-derived suppressor cells in aging by single-cell transcriptomics.npj aging · 2025Article
- Syndecan-1 Levels in Females with Active Rheumatoid Arthritis.Journal of clinical medicine · 2024Article
- Article
- Jintiange Capsule Alleviates Rheumatoid Arthritis and Reverses Changes of Serum Metabolic Profile in Collagen-Induced Arthritic Rats.Journal of inflammation research · 2021Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesRA is a chronic autoimmune disease characterized by joint inflammation and tissue destruction. Immune responses mediated by T cells and autoantibodies are known to play critical roles in RA. Collagen type II (CII)-induced arthritis (CIA) is a commonly used animal model of human RA. We have previously reported the identification of a new T cell inhibitory molecule CD300c. Here we investigate the ability of recombinant CD300c-IgG2a Fc (CD300c-Ig) fusion protein to prevent and treat CIA.
methodsMice were induced to develop CIA by CII and injected with CD300c-Ig or control Ig protein before or after CIA symptoms occur. The mice were examined for CIA clinical and pathological scores, and analysed for the expression of proinflammatory cytokines, the percentage and activation of CD4 T cells and regulatory T cells, CII-specific T cell proliferation and cytokine production, and CII-specific autoantibody production.
resultsIn a prevention model, CD300c-Ig significantly decreases CIA incidence, and reduces clinical and pathological arthritis scores. In the treatment model, CD300c-Ig ameliorates established CIA. The beneficial effects of CD300c-Ig are related to decreased expansion and activation of T cells in the spleen and reduced expression of proinflammatory cytokines in the joints. CD300c-Ig also inhibits CII-specific T cell proliferation and Th1 and Th17 cytokine production. In addition, CD300c-Ig treatment reduced the production of CII autoantibodies in the serum. Furthermore, CD300c-Ig inhibits the proliferation and activation of T cells from RA patients in vitro.
conclusionCD300c-Ig protein has the potential to be used in the treatment of patients with RA.
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