Chimeric antigen receptor T (CAR-T) cells are T cells engineered to express specific synthetic antigen receptors that can recognize antigens expressed by tumor cells, which after the binding of these antigens to the receptors are eliminated, and have been adopted to treat several kinds of malignancies. Autoimmune diseases (AIDs), a class of chronic disease conditions, can be broadly separated into autoantibody-mediated and T cell-mediated diseases. Treatments for AIDs are focused on restoring immune tolerance. However, current treatments have little effect on immune tolerance inverse; even the molecular target biologics like anti-TNFαinhibitors can only mildly restore immune balance. By using the idea of CAR-T cell treatment in tumors, CAR-T cell-derived immunotherapies, chimeric autoantibody receptor T (CAAR-T) cells, and CAR regulatory T (CAR-T) cells bring new hope of treatment choice for AIDs.

Introduction: This study aimed to assess the tumor risk of finerenone in individuals with type 2 diabetes mellitus (T2DM) aggravated by chronic kidney disease (CKD).Methods: A thorough search in the OVID Medline, OVID EMBASE, and Cochrane Library databases from their creation through 2 November 2022 yielded randomized controlled trials (RCTs) reporting on the tumor risks of finerenone in patients with T2DM complicated with CKD. A pair of reviewers selected the relevant studies based on selection criteria, collected data, and assessed the methodological quality of eligible RCTs. The Peto odds ratio (OR) with a 95% confidence interval (CI) was calculated, and subgroup analysis of tumor nature, tumor origin system, tumor origin organ, and follow-up time was performed. Furthermore, Egger’s test was implemented to determine publication bias.Results: Four RCTs with 14,875 participants who had a low-to-moderate risk of bias were included. Compared with placebo treatment, finerenone did not increase the risk of overall neoplasms (Peto OR = 0.97; 95% CI, 0.83–1.14), malignant neoplasms (Peto OR = 1.03; 95% CI, 0.86–1.23), benign neoplasms (Peto OR = 0.94; 95% CI, 0.50–1.80), or in situ neoplasms (Peto OR = 0.14; 95% CI, 0.01–2.17). Subgroup analysis of the tumor origin system showed that finerenone was associated with an increased risk of malignant neoplasms of urinary tract compared with placebo treatment (Peto OR = 1.69; 95% CI, 1.07–2.67). The results were found to be robust in sensitivity analysis, and there was no indication of publication bias. Discussion: Finerenone is not associated with an increased risk of overall tumors, but it may be linked to an increased risk of malignant neoplasms in urinary tract. Additional well-planned cohort studies in larger research populations are needed to corroborate these findings.Systematic Review Registration:https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022374101, Identifier CRD42022374101.

During the coronavirus disease 2019 (COVID-19) pandemic, convenient accessibility and rapid publication of studies related to the ongoing pandemic prompted shorter preparation time for studies. Whether the methodological quality and reporting characteristics of published systematic reviews (SRs)/meta-analyses are affected during the specific pandemic condition is yet to be clarified. This study aimed to evaluate the epidemiology, methodological quality, and reporting characteristics of published SRs/meta-analyses related to COVID-19. The Ovid Medline, Ovid Embase, Cochrane Library, and Web of Science electronic databases were searched to identify published SRs/meta-analyses related to the COVID-19 pandemic. Study screening, data extraction, and methodology quality assessment were performed independently by 2 authors. The methodology quality of included SRs/meta-analyses was evaluated using revised version of a measurement tool to assess SRs, and the reporting characteristics were assessed based on the preferred reporting items for SRs and meta-analyses guidelines. A total of 47 SRs/meta-analyses were included with a low to critically low methodological quality. The median number of days from the date of literature retrieval to the date that the study was first available online was 21 days; due to the limited time, only 7 studies had study protocols, and the studies focused on a wide range of COVID-19 topics. The rate of compliance to the preferred reporting items for SRs and meta-analyses checklists of reporting characteristics ranged from 14.9% to 100%. The rate of compliance to the items of protocol and registration, detailed search strategy, and assessment of publication bias was less than 50%. SRs/meta-analyses on COVID-19 were poorly conducted and reported, and thus, need to be substantially improved.

This study systematically analyzes the association between interleukin‐18 (IL‐18) gene polymorphisms and rheumatoid arthritis (RA) susceptibility. The electronic databases Ovid MEDLINE, Ovid Excerpta Medica Database, and Cochrane Library were searched to identify meta‐analyses that included case–control studies reporting IL‐18 gene polymorphisms and RA susceptibility. Data were reanalyzed using Review Manager Software 5.1, and Mantel–Haenszel random effects were applied for the five genetic models: allelic, recessive, dominant, homozygote, and heterozygote. The effect size of odds ratios (ORs) and their corresponding 95% confidence interval (CI) were calculated. A total of seven meta‐analyses with poor quality were included. The IL‐18 polymorphisms ‐607 A/C, ‐137 C/G, ‐920 T/C, and ‐105 C/A have been reported. With weak evidence, IL‐18 ‐607 A/C polymorphisms were associated with a reduced risk of RA susceptibility using the allele model (OR = 0.76, 95% CI: 0.61 − 0.93, p = 0.01), dominant model (OR = 0.67, 95% CI: 0.50 − 0.90, p = 0.008), homozygote model (OR = 0.57, 95% CI: 0.35 − 0.91, p = 0.02), and heterozygote model (OR = 0.71, 95% CI: 0.54 − 0.93, p = 0.01) in the overall population. IL‐18 gene polymorphisms and RA susceptibility are affected by ethnicity: With weak evidence, IL‐18 ‐137 C/G polymorphisms were related to reduce RA susceptibility in the Asian population (allele model: OR = 0.59, 95% CI: 0.40 − 0.88, p = 0.01; dominant model: OR = 0.57, 95% CI: 0.37 − 0.89, p = 0.01; heterozygote model: OR = 0.60, 95% CI: 0.38 − 0.94, p = 0.03). IL‐18 ‐607 A/C gene polymorphisms are a protective factor for RA susceptibility in the overall population, and IL‐18 −137 C/G gene polymorphisms are a protective factor for RA susceptibility in the Asian population. Further studies are needed to confirm these results owing to the limitations of the included studies.

Background. Insulin-like growth factor-binding proteins (IGFBPs) and connective tissue growth factor (CTGF) participate in angiogenesis. Dermatomyositis (DM) is characterized by microvasculopathy-derived skin lesions. Here, we investigated the clinical significance of serum IGFBP and CTGF levels in DM patients. Methods. In this study, 65 DM patients and 30 healthy controls were enrolled. Serum IGFBP and CTGF levels were examined by ELISA, and their correlation with clinical and laboratory findings was analyzed by Spearman’s correlation. Results. Serum IGFBP-2, IGFBP-4, and CTGF levels were higher in DM patients than in healthy controls (median (quartile): 258.9 (176.4–326.1) ng/mL vs. 167.7 (116.1–209.4) ng/mL, ; 450.4 (327.3–631.8) ng/mL vs. 392.2 (339.0–480.2) ng/mL, ; and 45.71 (38.54–57.45) ng/mL vs. 35.52 (30.23–41.52) ng/mL, , respectively). IGFBP-2 and CTGF levels were positively correlated with cutaneous ( , and , , respectively) and global ( , and , , respectively) disease activity in DM patients. Conclusion. Serum IGFBP-2 and CTGF levels were increased in patients with DM and correlated with cutaneous and global disease activity.