MiR-155-5p is a key oncogenic microRNA that maintains immune homeostasis and mediates crosstalk between inflammation and tumorigenesis. High expression of PD-L1 also plays an important role in immune tolerance in tumors. The aim of this study was to explore the relationship between miR-155-5p and PD-L1 in lung adenocarcinoma (LUAD) cells A549 and H1650. The expression levels of miR-155-5p and PD-L1 in LUAD patients were detected by RT-qPCR, and mimics of miR-155-5p were used to model increased expression in A549 or H1650 cells. After 24 h, we measured levels of PD-L1 by RT-qPCR, western blot and flow cytometry. In addition, we identified two sites in the PD-L1 3′-UTR (5′-AGCAUUA-3′ and 5′-GCAUUAA-3′) which can be bound by miR-155-5p using TargetScan. Compared with normal tissue, miR-155-5p was overexpressed in tumor tissue (P = 0.0456), while the expression of PD-L1 was not significantly different (P = 0.1349). The expression levels of miR-155-5p and PD-L1 were negatively correlated (r = -0.6409, P = 0.0459 and r = -0.7544, P = 0.0117). Exogenous overexpression of miR-155-5p decreased the mRNA, total protein and membrane protein expression levels of PD-L1 both in A549 and H1650 cells (P less then 0.05). MIF Antagonist Taken together, our data suggest that miR-155-5p may suppress the expression of PD-L1 in LUAD. This article is protected by copyright. All rights reserved.INTRODUCTION Lupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE), which is a chronic autoimmune disease. However, the detailed mechanisms underlying this disorder have remained unclear. Alpha2-antiplasmin (α2AP) is known to perform various functions, such as plasmin inhibition and cytokine production, and to be associated with immune and inflammatory responses. METHODS We investigated the roles of α2AP in the pathogenesis of LN using a pristane-induced lupus mouse model. RESULTS The levels of plasmin-α2AP complex and α2AP were elevated in the lupus model mice. In addition, α2AP deficiency attenuated the pristane-induced glomerular cell proliferation, mesangial matrix expansion, collagen production, fibrin deposition, immunoglobulin G deposition, and proinflammatory cytokine production in the model mice. We also showed that interferon-γ (IFN-γ), which is an essential inducer of LN, induced α2AP production through the c-Jun N-terminal kinase (JNK) pathway in fibroblasts. In addition, plasmin attenuated the IFN-γ-induced proinflammatory cytokine production through the AMPK pathway in macrophages, and α2AP eliminated these effects. Furthermore, we showed that α2AP induced proinflammatory cytokine production through the ERK1/2 and JNK pathways in macrophages. CONCLUSION α2AP regulates the inflammatory responses through plasmin inhibition and proinflammatory cytokine production and is associated with the development of LN. Our findings may be used to develop a novel therapeutic approach for SLE. © 2020 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd.Glioblastoma multiforme (GBM) and primary central nervous system lymphoma (PCNSL) are both malignant cerebral tumors; however, their treatments are vastly different. Early and precise diagnosis is vital for subsequent adequate treatment to improve prognosis. Reliable biomarkers that can easily distinguish GBM and PCNSL are urgently needed. We evaluated the diagnostic potential of lymphocyte-specific protein tyrosine kinase (LCK) as a biomarker in differentiating PCNSL from GBM using established computational approaches (Gene Expression Profiling Interactive Analysis, The Cancer Proteome Atlas, Tumor Immune Estimation Resource, GEO, Oncomine) and immunohistochemistry. The results showed that LCK was expressed at a high level in PCNSL patients but at a low level in GBM patients. Moreover, LCK expression positively correlated with the levels of infiltrating B cells in diffuse large B-cell lymphoma (DLBCL) and GBM. Overall, bioinformatics analysis and immunohistochemistry revealed that LCK expression is a potential biomarker for distinguishing PCNSL from GBM. © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.OBJECTIVE Yangxue Qingnao granules (YXQNG), which translates to granules that tonify the blood and clear liver heat, are widely available in China for the treatment of Chronic Cerebral Circulation Insufficiency (CCCI). This systematic review aimed to evaluate the effectiveness and safety of YXQNG in treating CCCI. METHODS PubMed, the Cochrane Central Register of Controlled Trials, Embase, the Chinese National Knowledge Infrastructure, and the Wanfang Database were searched from their inception to February 2019. Randomized controlled trials of YXQNG used alone or in combination with other drugs against a placebo, with no intervention or used with other drugs in CCCI patients were identified. The reviewers identified studies, extracted data, and assessed the quality of the evidence, independently and in duplicate. The Cochrane risk of bias assessment tool was used for quality assessment. RESULTS A total of 31 RCTs and 2,877 patients were selected. The meta-analysis indicated that the ratio between the combined RR of the total effective rate and the 95% confidential interval (95% CI) was 1.21 (1.17, 1.26). The combined MD of transcranial Doppler (TCD) detecting carotid artery, vertebral artery, and basilar artery blood flows (95% CI), respectively, were 8.84 (5.83, 11.85), 4.72 (3.71, 5.73), and 3.89 (3.03, 4.76). The combined MD of plasma viscosity and fibrinogen, respectively, were -0.35 (-0.40, -0.30) and -0.81 (-1.12, -0.50). Serious adverse effects were not reported in all the included trials. CONCLUSION This systematic review revealed that YXQNG could increase cerebral blood flow in patients with CCCI and improve their symptoms, with no serious adverse effects. Since the literature reviewed was affected by factors such as lower quality of the included studies, the systematic evaluation’s conclusion is not very reliable. Thus, more rigorously designed trials are needed. © 2020 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.