The prevalence of obesity has been increasing in the last few decades, and it is regarded as one of the major health problems in the world. The rising prevalence of obesity in children and adults is a result of eating disorders and the changes related to the modern lifestyle. Obesity alters the adipocytes’ substance secretion, which affects the function of the immune system and leads to obesity-induced inflammation and the development of obesity-related cancers. Altered chemokines, adipokines, and conditions like insulin resistance are most likely related to the impaired immune system in the obesity state. The impaired secretion of adipokines, such as increased leptin and reduction in adiponectin, affects innate immune system antitumor responses after long-term exposure. In addition, changes in chemokines and, consequently, the promotion of insulin resistance create an immunosuppressive environment that debilitates the host to fight against tumor growth, progression, and metastasis. Accordingly, it may increase cancer susceptibility in obese individuals. Thereby, it can be concluded that treatment of obesity will greatly affect the improvement of immune system function and, as a result, may possibly reduce the risk of cancer. The aim of this study is to review the pathways resulting in impaired immune system and inflammation and their link to cancer progression in obesity. Several hypotheses have been proposed to have a critical contribution to the development of obesity-related cancers, such as the function of cytokines, insulin resistance, and NF-κB and senescence changes in obesity. These hypotheses will be discussed later in this article.

As a pro-inflammatory cytokine, IL-17 is important in the immune system against fungal and bacterial infections. The IL-17 cytokine family consists of six members that exert their effects by cooperating with five receptors that form the IL-17 receptor family. Although IL-17 is mainly a defensive factor, at times, overexpression of this cytokine will lead to inflammatory and damaging outcomes.
Pneumonia is a lower airway disease that can be caused by different agents. In this condition, IL-17 is secreted from different cells and can fight against infection or otherwise lead to progression of the disease. This article reviews the IL-17 role in pneumonia and different inflammatory pathways that it can affect.

Rituximab is a chimeric monoclonal antibody with binding specificity to CD20-positive B lymphocytes. Patients administered rituximab would not have adequate humoral response to the SARS-CoV-2 vaccine. Rituximab can also affect the durability of immunization. Plasma-secreting antibodies and memory B-cells are two major arms of long-term immunity. The role of memory B-cells becomes prominent by decreasing antibody titers over time. The activated memory B cells have CD20 protein on their surface. Investigating the effect of rituximab on other vaccines has demonstrated attenuated recall response. The evidence in this review suggests that we can also expect a deficit of recall response to SARS-CoV-2, making the rituximab-treated patients susceptible to reinfection with emerging variants. Therefore, it is better to consider other therapeutic options, use lower rituximab doses, and employ booster vaccines at shorter intervals.

Infectious diseases, which are caused by microorganisms such as bacteria, viruses, fungi, or parasites, can be contracted from other people, the environment, animal contact, or insect bites. Infectious diseases are becoming escalating concerns, mainly due to increasing antibiotic resistance. These disorders remain one of the primary causes of human mortality. Due to the lack of human data on new emerging diseases, ethical values, and the lethal risk of these pathogens, animal models are often recommended for experimental research on these diseases. According to the similarities between humans and animals in physiology, genetics, anatomy, availability, ease of handling, and production rate, scientists evaluate different medical problems in animal models before applying their findings to humans. According to the recent advent of the isolation of novel microorganisms, researchers must challenge the infectious ability of microorganisms in the biological system of animal models. An infectious disease animal model attempts to mimic the host-pathogen interaction. Accordingly, a disease model is defined by both the host and pathogen combination. In this review article, we aimed to discuss various animal models established for studying different infectious diseases.

A stroke is an enervating injury to the brain that occurs from a stoppage in blood supply (ischemic stroke) or bleeding (hemorrhagic) in a hemisphere of the brain. Globally, about 10 million deaths per year are recorded because of stroke. There has been no definitive FDA-approved treatment for chronic ischemic stroke without any side effects so far. Therefore, the search for new therapies is necessary. In this paper, after investigating several studies online, on Google Scholar, PubMed, and Scopus, we hypothesized improving the complications of chronic ischemic stroke in induced Sprague-Dawley rat model by intraluminal suture middle cerebral artery occlusion (MCAo), utilizing the combination of cell therapy and gene therapy.
A new version of astrocytes is proposed by making some changes in their genome. To gain this goal, a gene profile including IL-38 (the most modern anti-inflammatory agent, which barricades inflammatory response factors), BRAG-1 (an anti-apoptotic gene from BCL-2 family), IL-38 and BRAG-1’s complementary scaffold RNAs for their expression by deadCas9 (dCas9), complementary scaffold RNAs of LZK and MST-1 for their deletion, and deadCas9 gene is used.
Based on studies and documents, we hypothesized using modified astrocytes by dCas9, which is the most accurate genome-editing technology

Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by diverse behavioral and cognitive challenges. Despite its rising prevalence, the underlying mechanisms remain inadequately understood. Toll-like receptors (TLRs), as critical components of the innate immune system, are implicated in neuroinflammatory processes that may contribute to the pathogenesis of ASD. This narrative review delves into the relationship between TLRs and ASD. Notably, studies reveal an upregulation of TLR4 and TLR2 expression in B cells and placental tissues of individuals with ASD, correlating with increased levels of pro-inflammatory cytokines such as IL-6 and TNF-alpha. Maternal immune activation (MIA), particularly due to infections during pregnancy, has been shown to trigger TLR-mediated inflammatory responses that adversely affect fetal brain development. For instance, maternal cytomegalovirus (CMV) infection leads to heightened expression of TLR4/2 in the placenta, resulting in significant placental inflammation and altered neurodevelopmental trajectories in offspring. Furthermore, evidence indicates that individuals with ASD exhibit impaired immune responses characterized by dysfunctional natural killer (NK) cells and monocytes, which produce excessive pro-inflammatory cytokines upon TLR4 stimulation but show diminished responses to TLR9 ligands. This immune dysregulation is associated with a shift towards a TH2 cytokine profile, complicating the understanding of immune phenotype correlations with ASD symptom severity. Additionally, TLR3 activation by viral RNA has been linked to behavioral changes in murine models, underscoring the potential for maternal infections to influence neurodevelopment through TLR signaling pathways. These findings illuminate the role of TLRs in ASD pathophysiology and suggest that targeting TLR pathways may offer novel therapeutic avenues for intervention in this complex disorder.

Background

Recurrent Aphthous Stomatitis (RAS) is a common and painful condition characterized by recurrent ulcers in the oral mucosa, affecting a significant portion of the population and leading to considerable discomfort and decreased quality of life. Despite its prevalence, the underlying etiology of RAS remains poorly understood, with factors such as genetics, immune dysregulation, and environmental triggers being implicated. C-reactive protein (CRP) is an acute-phase protein primarily produced by the liver in response to inflammation, and its levels in serum can serve as a biomarker for systemic inflammatory conditions. This study aims to investigate the relationship between serum CRP levels and the occurrence of RAS seeking to elucidate the role of systemic inflammation in this condition.

Methods

In a cross-sectional study design, we enrolled 26 participants diagnosed with RAS according to established diagnostic criteria, alongside a control group of 26 healthy individuals matched for age and gender. Serum CRP levels were quantified using enzyme-linked immunosorbent assay (ELISA) methods, and demographic, clinical, and lifestyle data were collected through structured questionnaires. We employed statistical analyses, including t-tests and regression models, to assess the association between serum CRP levels and the frequency and duration of RAS.

Results

Our findings reveal significantly elevated serum CRP levels in individuals with RAS compared to healthy controls (p<0.04), indicating a potential link between systemic inflammation and the pathophysiology of RAS. Additionally, elevated CRP levels were associated with increased ulcer severity and prolonged healing time. Multivariate analyses further demonstrated that serum CRP could serve as an independent predictor of RAS severity, highlighting its potential role as a biomarker for disease activity.

Conclusion

In conclusion, our investigation provides compelling evidence that systemic inflammation, as indicated by elevated serum CRP levels, is associated with RAS.

Background: The role of immune dysfunction in migraine pathogenesis is currently debated. Migraines are common among family members, yet no significant gene polymorphisms have been identified to date. However, our earlier clinical study findings led us to hypothesize that migraine initiation could be influenced by genes that regulate immune function, specifically Forkhead box P3 (FOXP3). To test this hypothesis, we conducted a pilot study targeting FOXP3 Single Nucleotide Polymorphisms (SNPs), commonly associated with other autoimmune conditions in patients with migraine. Materials and Methods: The minimum sample size required for this study was determined by considering the mean difference in Regulatory T cells (Tregs) reduction reported in previous studies. Twenty participants (10 patients and 10 controls) were recruited for this study. Familial clinical history was collected for pedigree analysis and the samples were tested for the targeted SNPs. Results: The prevalence of the AG genotype for rs2232365 was 50% among patients and 20% among controls (OR: 4.0, CI: 0.54-29.09, p=0.17). Regarding rs3761547, the AG genotype was observed in 60% of patients and 10% of controls (OR: 13.5, CI: 1.19-152.2, p=0.03), whereas the AC genotype was found in 70% of patients and only 10% of controls (OR: 21.0, CI: 1.77-248.1, p=0.01). Conclusion: Our preliminary analysis suggested a possible association between FOXP3 variance and migraine predisposition, particularly with the AG and AC genotypes at the rs3761547 and rs3761548 SNPs, respectively. These findings highlight the importance of conducting a more extensive FOXP3 mutation study in a larger cohort of migraine patients.