Objective: Anti-MDA5 antibody-positive dermatomyositis (DM) is a rare clinical autoimmune disease, and anti-MDA5-positive DM with interstitial lung disease (ILD) is the most important cause of death in DM patients. We reported the efficacy of the JAK1/3 inhibitor tofacitinib as an anti-MDA5negative treatment option for patients with anti-MDA5-positive DM-ILD. Method and process: Here we report a 51-year-old female patient with cough, sputum, shortness of breath for 5 months, rash for 3 months, and muscle pain in the extremities for 1 month. After conventional immunosuppressive therapy plus hormone therapy, the remission was slow.Methylprednisolone was successfully reduced after we administered tofacitinib and tacrolimus. After 132 weeks of follow-up, anti-MDA5 antibody turned negative, clinical symptoms were relieved, and lung Imaging tests were successfully reversed. Results and Conclusion:There is currently no report of tofacitinib supplement therapy for anti-MDA5 positive to negative DM. With this case report, tofacitinib is an option for the treatment of anti-MDA5-positive DM-ILD, which deserves attention.
Infiltration and aggregation of lymphocytes in exocrine glands are the basic pathological manifestations of Sjögren’s syndrome (SS), and the incidence of SS has been increasing year by year in recent years. To explore the potential signaling pathway of Runzaoling (RZL) in alleviating SS, the possible targets of RZL in SS were firstly explored through network pharmacology, and then, the regulation of PI3K/AKT/mTOR signaling in NOD mice and Th17 cells was verified. 75 8-week-old NOD mice were casually classified into 5 groups: model; hydroxychloroquine; high, medium, and low dose RZL groups, with 15 in each; and 15 BALB/c mice were employed as control group. After 10 weeks of continuous intragastric administration in mice and 24 hours of drugs intervention in Th17 cells, histopathology was observed by HE staining, and the gene transcription levels were identified by real-time quantitative PCR (RT-qPCR). The protein expressions were detected by western blotting (WB). The findings showed that high and medium dose RZL group could attenuate the submandibular gland tissue damage. The results indicated that the mRNA expressions of PI3K, AKT, mTOR, STAT3, and IL-17 in SS mice and in IL-17 stimulation of Th17 cells were dramatically increased compared with control group and decreased to varying degrees after RZL intervention. The trend of phosphorylated PI3K/AKT/mTOR and STAT3 and IL-17 protein expression in NOD mice and Th17 cells were consistent with mRNA. RZL can downregulate STAT3 and IL-17 expressions in the submandibular gland of NOD mice and in Th17 cells via regulating the PI3K/AKT/mTOR signaling pathway. Moreover, RZL could reduce the activation of CD4+ T lymphocyte differentiation to Th17 cells.
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