Regular ArticleImmune Function in Patients with Rheumatoid Arthritis Treated with Etanercept
References (35)
- et al.
Infliximab induces apoptosis in monocytes from patients with chronic active Crohn's disease by using a caspace-dependent pathway
Gastroenterology
(2001) - et al.
The neutrophil in rheumatoid arthritis
Rheum. Dis. Clin. North Am.
(1995) - et al.
Tumor necrosis factor and lymphotoxin
Cytokines
(1998) - et al.
Cytokines
Basic and Clinical Immunology
(1991) - et al.
Detection of tumor necrosis factor α but not tumor necrosis factor β in rheumatoid arthritis synovial fluid and serum
Arthritis Rheum.
(1988) - et al.
Localization of tumor necrosis factor α in synovial tissues and at the cartilage-pannus junction in patients with rheumatoid arthritis
Arthritis Rheum.
(1991) - et al.
Soluble tumor necrosis factor (TNF) receptors are effective therapeutic agents in lethal endotoxemia and function simultaneously as both TNF carriers and TNF antagonists
J. Immunol.
(1993) - et al.
A comparison of etanercept and methotrexate in patients with early rheumatoid arthritis
N. Engl. J. Med.
(2000) - et al.
Etanercept in children with polyarticular juvenile rheumatoid arthritis
N. Engl. J. Med.
(2000) - et al.
Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein
N. Engl. J. Med.
(1997)
Etanercept therapy in rheumatoid arthritis. A randomized, controlled trial
Ann. Intern. Med.
A trial of etanercept, a recombinant tumor necrosis factor receptor: Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate
N. Engl. J. Med.
The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis
Arthritis Rheum.
Determinants of neutrophil HOCl generation: Ligand-dependent responses and the role of surface adhesion
J. Leukocyte Biol.
Differences in the ingestion mechanisms of IgG and C3b particles in phagocytosis by neutrophils
Immunology
Deactivation of vascular endothelium by monoclonal anti-tumor necrosis factor α antibody in rheumatoid arthritis
Arthritis Rheum.
In vivo blockade of TNF-α by intravenous infusion of a chimeric monoclonal TNF-α antibody in patients with rheumatoid arthritis
J. Immunol.
Cited by (61)
miR-22 inhibits synovial fibroblasts proliferation and proinflammatory cytokine production in RASF via targeting SIRT1
2020, GeneCitation Excerpt :Some studies have found that the pathogenesis of RA may involve local microenvironment factors, multiple gene regulation, and other random factors, but the etiology of RA has not been fully elucidated (Kurko et al., 2013). Studies have shown that the inflammatory response in patients with RA is associated with congenital and acquired immune function, and the use of anti-protein drugs has a specific therapeutic effect on patients with RA (Moreland et al., 2002; Cordain et al., 2000). Therefore, targeting inflammation in patients with RA is one of the key research directions in RA therapy.
Novel aspects of the activation of NADPH oxidase in neutrophils of rheumatic patients on biological therapy
2019, International ImmunopharmacologyCitation Excerpt :An increased ROS formation was observed by Capsoni et al. [39] in isolated neutrophils of rheumatic patients receiving adalimumab therapy. In other studies, the biological therapy did not exert any effect [20,40,41], yet none of these investigations included a separate detection of extra- and intracellular ROS. The antibodies against TNFα or IL-6 receptor increased the intracellular but not extracellular chemiluminescence.
Neutrophils
2016, Kelley and Firestein's Textbook of Rheumatology: Volumes 1-2, Tenth EditionThe Comparative Safety of Tumor Necrosis Factor Inhibitors in Rheumatoid Arthritis: A Meta-analysis Update of 44 Trials
2014, American Journal of Medicine
- 1
To whom correspondence should be addressed, Larry W. Moreland, MD at Arthritis Clinical Intervention Program, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, 17176th Ave. S, Room 068, Birmingham, AL 35294-7201. Fax: (205) 975-5554. E-mail: [email protected].