Introduction: Lupus nephritis (LN) is one of the most severe signs of systemic lupus erythematosus (SLE) and rapid diagnosis of kidney damage remains an important concern for LN. Objectives: The aim of this study was to investigate the association of the serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and interleukin 17 (IL-17) with SLE severity, renal involvement, and other clinical manifestations in lupus patients. Patients and Methods: In order to determine a better biomarker for the detection of renal damage, this study evaluated the ability of serum TWEAK (sTWEAK) and IL-17 in lupus patients with (n=25) and without (n=25) nephritis and healthy controls (n=39). Moreover, it compared the levels of these cytokines with disease activity and chronicity as well as traditional serum markers including complement C3 and C4, creatinine, and proteinuria in lupus patients. Results: Increased levels of sTWEAK and IL-17 were observed in SLE and LN groups compared to healthy controls and non-LN groups, respectively. Significant positive associations were observed between serum TWEAK and IL-17 levels and systemic lupus erythematosus disease activity index (SLEDAI), proteinuria, nephritis activity index, and some clinical manifestations (P<0.05). Discriminating the ability of the studied cytokines were not better than the utility of any markers individually. Conclusion: The serum levels of TWEAK and IL-17 in the SLE and LN groups were significantly higher than the control group and both markers were indicative of the renal disease severity; therefore, they could possibly indicate renal involvement in the lupus patients.

Introduction: COVID-19 (coronavirus disease 2019) was identified in China in December 2019 for the first time and is rapidly spreading throughout the world as a pandemic. As COVID-19 causes mild to severe acute respiratory syndrome, most studies in this context have focused on pathogenesis primarily in the respiratory system. However, evidence shows that the central nervous system (CNS) may also be affected by COVID-19. Since COVID-19 is spreading, it is imperative to study its possible cognitive effects in patients suffering and recovering from COVID-19. Methods: The articles used in this study were searched by keywords such as Cytokine storm and covid-19, covid-19 and executive dysfunction, cognitive disorder and covid-19, CNS and covid 19, Coronavirus, Neuroinvasion in science direct, Scopus, PubMed, Embase, and Web of Science databases based on Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) checklist. The study will assess all observational studies published between December 2019 and April 2021 in peer-reviewed journals, including cross-sectional, cohort, case-control studies, case reports and case series. The search result was 106 articles, of which 73 articles related to Covid-19, the stages of infection by this virus, its effect on the nervous system and neurological symptoms, the cytokine storm caused by this infection, and the possible cognitive consequences caused by this virus in patients, has been reviewed. Other articles were not checked due to their limited relevance to the topic under discussion. Results: Studies show that neurons may be directly affected by SARS-CoV-1 and SARS-CoV-2. Furthermore, various studies indicate that systemic inflammation (so-called "cytokine storm") is also responsible for brain damage induced by infection with SARS-CoV-1 and SARS-CoV-2. Such a way that this patients showed elevated levels of interleukin (IL-), 6, 8, and 10 and of tumor necrosis factor-alpha (TNF- α) in their blood. Conclusion: Various cognitive defects following an increase level of cytokines such as TNF-α and IL-6,8 have been observed. Therefore, due to the increase level of these pro-inflammatory factors in the brains of these patients, cognitive deficits can be expected, which need further investigation.