Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rifamycin SV, injected intraarticularly at dosages of 500 mg weekly, induced a complete removal of persistent knee effusions in 57 of 60 rheumatoid patients, and in all patients with effusions due to juvenile rheumatoid arthritis (three), ankylosing spondylitis (three), psoriatic arthritis (10), intermittent hydrarthrosis (two) and chondromatosis (two). One rheumatoid patient did not respond to treatment, and two dropped out because of local side effects. The number of infiltrations varied between three and 12, and was correlated with activity grade of local synovitis (P < .05). As of this writing, 50 out of 57 rheumatoid patients and 19 out of 20 belonging to the other groups have not had a relapse of effusions after 25 to 36 months and 12 to 20 months respectively. While the changes in the synovial fluid and membrane of the rheumatoid subjects, and the results obtained from experimental arthritis in guinea pigs, confirm the hypothesis that Rifamycin has a local antiinflammatory action in arthritic knee joints, they also suggest that this property alone of the drug is not entirely responsible for its therapeutic action.
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PMID:Rifamycin SV in the Treatment of Knee Synovitis. 2483 10

Ankylosing spondylitis (AS) is a chronic autoimmune inflammatory disease with severe inflammatory symptoms in the axial skeleton. The cause of ankylosing spondylitis is unknown. TNFAIP3, also named A20, uses ubiquitin-related functions to regulate immune activation, deficiency of which is highly related to autoimmune disease. However, the role of TNFAIP3 in human AS has not been reported. Our objective was to study the role and mechanism of TNFAIP3 in ankylosing spondylitis. TNFAIP3 expression on different types of immunocytes from AS peripheral blood was measured by flow cytometry. In vitro, monocytes were transfected with a TNFAIP3 shRNA lentivirus, and IL6 and IL1B activation was tested using real-time PCR and ELISA. The novel interaction complex TNFAIP3-DEPTOR was determined through GST pull-down, yeast two-hybrid system, confocal microscopy, and co-immunoprecipitation. Transmission electron microscopy, the RFP-GFP-LC3 adenovirus, and LC3 expression were used for autophagy detection. Here, we show that TNFAIP3 expression in AS peripheral blood non-classical monocytes was decreased. In normal monocytes, TNFAIP3 induced autophagy, which restricted inflammasome activation to the early stage of LPS stimulation. Zinc-finger domains of TNFAIP3 were able to interact and stabilize DEPTOR. TNFAIP3 and DEPTOR together rapidly promoted autophagy after LPS treatment to prevent NLRP3 inflammasome formation. Finally, TNFAIP3 and DEPTOR deficiency in AS non-classical monocytes facilitated inflammasome activation. Our study indicates that TNFAIP3-DEPTOR complex-induced early-onset autophagy is vital for immune inhibition in autoimmune disease.
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PMID:TNFAIP3-DEPTOR complex regulates inflammasome secretion through autophagy in ankylosing spondylitis monocytes. 2994 Aug