ArticleAnnals of the rheumatic diseases2004
Anti-CD4 monoclonal antibody treatment in acute and early chronic antigen induced arthritis: influence on macrophage activation.
Article in Annals of the rheumatic diseases, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Periarticular myositis and muscle fibrosis are cytokine-dependent complications of inflammatory arthritis.JCI insight · 2025Article
- Recent advances in development of nano-carriers for immunogene therapy in various complex disorders.Iranian journal of basic medical sciences · 2022Review
- Molecular Approaches for the Treatment of Pompe Disease.Molecular neurobiology · 2020Review
- Enhanced efficacy from gene therapy in Pompe disease using coreceptor blockade.Human gene therapy · 2015Article
- AMPA/kainate glutamate receptors contribute to inflammation, degeneration and pain related behaviour in inflammatory stages of arthritis.Annals of the rheumatic diseases · 2015Article
- Glucocorticoid therapy of antigen-induced arthritis depends on the dimerized glucocorticoid receptor in T cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Loss of phosphoinositide 3-kinase gamma decreases migration and activation of phagocytes but not T cell activation in antigen-induced arthritis.BMC musculoskeletal disorders · 2010Article
- Chitosan/siRNA nanoparticle-mediated TNF-alpha knockdown in peritoneal macrophages for anti-inflammatory treatment in a murine arthritis model.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
- In vitro model for the analysis of synovial fibroblast-mediated degradation of intact cartilage.Arthritis research & therapy · 2009Article
- Distinct in vivo roles of CD80 and CD86 in the effector T-cell responses inducing antigen-induced arthritis.Immunology · 2008Article
- Biological therapies directed against cells in autoimmune disease.Springer seminars in immunopathology · 2006Review
- Immune tolerance to cardiac myosin induced by anti-CD4 monoclonal antibody in autoimmune myocarditis rats.Journal of clinical immunology · 2006Article
- Attenuation of murine antigen-induced arthritis by treatment with a decoy oligodeoxynucleotide inhibiting signal transducer and activator of transcription-1 (STAT-1).Arthritis research & therapy · 2006Article
- Expression of cytokine mRNA and protein in joints and lymphoid organs during the course of rat antigen-induced arthritis.Arthritis research & therapy · 2005Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the indirect effects of anti-CD4 treatment on the functions of macrophages (CD4(-) in mice) in the acute and early chronic phase of mouse antigen induced arthritis (AIA).
methodsC57BL/6 mice with AIA were treated intraperitoneally with the anti-CD4 mAb GK1.5 or control rat IgG on days -1, 0, 1, 3, 5, and 7. Proinflammatory cytokines (IL1 beta, IL6, and TNF alpha) were quantified by sandwich ELISA in joint extracts, serum, and supernatants of ex vivo stimulated spleen/lymph node cells or peritoneal macrophages (+LPS/IFN gamma). Nitric oxide (NO) levels in supernatants of ex vivo stimulated peritoneal macrophages were measured by the Griess reaction. Proteolytic activity in joint homogenates was analysed by gelatin, casein, and elastin zymography, and substrate assays.
resultsAnti-CD4 treatment significantly reduced joint swelling in acute (days 3, 5) and early chronic AIA (day 7) and diminished inflammation and destruction scores in late chronic AIA (day 21). On day 3, anti-CD4 treatment significantly reduced IL6 levels in all compartments. IL1 beta was reduced in joint extracts, unaffected in serum or cells from lymphoid organs, and increased in stimulated peritoneal macrophages. TNF alpha was significantly increased in the joints, decreased in serum, and otherwise unchanged. NO production by stimulated peritoneal macrophages was significantly reduced by anti-CD4 treatment. Lower activity of matrix metalloproteinases and neutrophil elastase was seen in joint extracts of anti-CD4 treated animals than in IgG treated AIA controls.
conclusionCD4(+) T cell directed treatment had strong local and systemic effects on macrophages. These indirect effects may contribute to the reduction of destructive mediators/joint destruction in AIA.
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