The mouse/human chimeric anti-CD20 Rituximab(Moab mabthera) can avoid acting on stem cells,pre-B cells and plasma cells;and selectively targets on B cells which have CD20 on their surfaces.Rituximab has been shown to reduce signs and symptoms and to slow the progression of structural damage in adult patients with moderately-to severely-active rheumatoid arthritis in randomised controlled trials and now in the United States has been approved for use in combination with methotrexate(MTX)for the treatment of rheumatoid arthritis by the US Food and Drug Administration.

Malignant lymphoma complicated by Behcet's disease (BD) is a rare clinical entity. We report a case of BD complicated by malignant lymphoma in a 26-year-old male patient. The patient was diagnosed to have terminal ileum extranodal NK/T-cell lymphoma (nasal type) during treatment for BD with cyclophosphamide (CTX), immunoregulants and biological agents. This is the first case reported in China and the second case globally. The pathogenesis of BD complicated by malignant lymphoma remains unclear. We reviewed the relevant literatures to summarize the clinical characteristics of BD complicated by extranodal NK/T-cell lymphoma (nasal type) and discuss the possible pathogenesis in light of immunology, EB virus infection and medications.
Adult ; Behcet Syndrome ; complications ; Humans ; Lymphoma, Extranodal NK-T-Cell ; complications ; Male

Objective To study the clinical characteristics and analyze the correlative risk factors of interstitial pneumonia in systemic lupus erythematosus (SLE-IP).Methods 80 SLE patients in department of rheumatology of Nanfang hospital form January 2013 to January 2016 were retrospectively analyzed.SLE patients with interstitial pneumonia (n=40) were divided into case group.40 cases of SLE with interstitial pneumonia were selected and matched with age and sex.Patients with mild SLE without interstitial pneumonia were treated as controls.The clinical manifestations,routine examination,biochemical examination and immunological examination were performed to compare the risk factors of SLE-related interstitial pneumonia.Results In this study,non-specific interstitial pneumonia (NSIP) and usual interstitial pneumonia (UIP) were common in SLE-IP patients.the ground-glass opacities were more common in NSIP type,while Grid shadows and honeycomb shadows were more common in UIP type.The dry cough,chest tightness / shortness of breath,Raynaud's phenomenon,wet rales,triglyceride increased,anti-Sm antibody positive rate,anti-U1-nRNP positive rate between two groups were statistically significant (P＜0.05).Logistic regression analysis showed that the risk factors of SLE-IP were dry cough,chest tightness / shortness of breath,Raynaud's phenomenon,wet rales,triglyceride increased,anti-Sm antibody positive and anti-U1-nRNP positive.Conclusion The presence of dry cough,chest tightness / shortness of breath,Raynaud's phenomenon,wet rales,triglyceride increased,anti-Sm antibody positive and anti-U1-nRNP positive all suggest the probability of interstitial pneumonia in SLE patients.HRCT plays an important role in the diagnosis of interstitial pneumonia in lupus,which is valuable to improve the prognosis.

Objective To investigate the mechanism of leflunomide (LEF) in regulating pulmonary fibrosis by regulating microRNA (miR)-449a. Methods Human lung fibroblasts MRC-5 were divided into 6 groups: control group, LEF group, LEF+mimic group, mimic group, LEF+inhibitor group and inhibitor group. MiR-449a was overexpressed or silenced by plasmid transfection with miR-449a mimic or inhibitor and ncubate for 48 h at 5 mg / L LEF. The cell viability, cell proliferation ability and apoptotic rate of each group were measured by CCK-8 method, clone formation experiment and flow cytometry. Immunofluorescent staining was used to detect α smooth muscle actin (α-SMA) and collagen I (col I). The levels of miRNA and protein were detected using qPCR and Western blot, respectively. Results The miR-449a level in the mimic group was significantly higher than that in the control group (P<0.05). The level of miR-449a in LEF group and inhibitor group was significantly lower than that in control group (P<0.05). The expression level of miR-449a in LEF+mimic group was significantly higher than that in LEF group, and the level of miR-449a in LEF+inhibitor group was significantly lower than that in LEF group (P<0.05). The cell viability and cell proliferation ability of the LEF group and inhibitor group were significantly higher than those of the control group (P<0.05). The cell viability and cell proliferation ability of the mimic group were significantly lower than those of the control group (P<0.05). The cell viability and cell proliferation ability of the LEF+mimic group were significantly lower than those of the LEF group, while the cell viability of the LEF+inhibitor group was significantly higher than that of the LEF group (P<0.05). The apoptosis rate of LEF group and inhibitor group was lower than that of control group (P<0.05). The apoptosis rate of mimic group was significantly higher than that of control group (P<0.05). The apoptosis rate of LEF+mimic group was significantly higher than that of LEF group, while the apoptosis rate of LEF+inhibitor group was significantly lower than that of LEF group (P<0.05). The fluorescence intensity of α-SMA and Col I proteins in LEF group and inhibitor group were significantly higher than those in control group (P<0.05). The relative fluorescence intensity of mimic group was lower than that of control group (P<0.05). The relative fluorescence intensities of α-SMA and Col I proteins in LEF+mimic group were significantly lower than those in LEF group, while the relative fluorescence intensities of α-SMA and Col I protein in LEF+inhibitor group were significantly higher than those in LEF group (P<0.05). The levels of p-JNK / JNK in LEF group and inhibitor group were higher than those in control group (P<0.05). The p-JNK / JNK level in the mimic group was significantly lower than that in the control group (P<0.05). The level of p-JNK / JNK in LEF+mimic group was significantly lower than that in LEF group, while the level of p-JNK / JNK in LEF+inhibitor group was significantly higher than that in LEF group (P<0.05). Conclusion LEF may activate the JNK pathway by inhibiting the expression of miR-449a in lung fibroblasts, thereby inducing fibroblast activation and proliferation, inhibiting apoptosis, and causing pulmonary fibrosis.