BACKGROUND: International guidelines recommend a pathway for preferable nursing handling in a specific cancer topic, like chemotherapy toxicity, low adhesion in toxicity reported with a consequential increase in adverse events (AEs) frequency, poorer QoL outcomes, and increased use of healthcare service until death. Unpredictability, postponed reports, and incapability to access healthcare services can compromise toxicity-related effects by including patients\' safety. In this scenario, a more attentive nursing intervention can improve patients\' outcomes and decrease costs for healthcare services, respectively. The present scoping review aims to describe and synthesize scientific care nursing evidence assessment in oncology patients.
METHODS: PubMed, Embase, Nursing & Allied Health Database, and British Nursing were the databases examined. Keywords used and associated with Boolean operators were assessment, care, nursing, immune disorder, oncology, and patient. Research articles considered were published between 2013-2023. All systematic processes were performed according to the PRISMA procedure in order to reach all manuscripts considered in the present scoping review.
RESULTS: The Embase database showed a total of 25 articles, PubMed displayed 77, the Nursing & Allied Health Database evidenced a total of 74, and the British Nursing database showed 252 records. Then, after a first revision in each database by considering the inclusion criteria, the abovementioned titles and abstracts were selected and, 336 records were removed, and 92 studies remained. Of these, 65 manuscripts were excluded after verifying abstracts. Finally, a total of 7 articles were carefully analysed and selected for this scoping review. Specifically, 2 articles belonged to the British Nursing Database, 3 articles belonged to Embase, 1 to the Nursing & Allied Health Database and one related to PubMed.
CONCLUSIONS: Oncology nursing should consider several aspects, such as therapy-related toxicity and its related morbidity and mortality, worsening levels of quality of life, and increasing duty by the healthcare organization or endorsements for the principal symptoms and signs which may anticipate few diseases and worst clinical conditions, too. Therefore, careful monitoring may allow prompt recognition and subsequent earlier management in the treatment efficacy.

Regulatory T cells (Tregs) are crucial in regulating T-cell-mediated immune responses. Numerous studies have shown that dysfunction or decreased numbers of Tregs may be involved in inflammatory cardiovascular diseases (CVDs) such as atherosclerosis, hypertension, myocardial infarction, myocarditis, cardiomyopathy, valvular heart diseases, heart failure, and abdominal aortic aneurysm. Tregs can help to ameliorate CVDs by suppressing excessive inflammation through various mechanisms, including inhibition of T cells and B cells, inhibition of macrophage-induced inflammation, inhibition of dendritic cells and foam cell formation, and induction of anti-inflammatory macrophages. Enhancing or restoring the immunosuppressive activity of Tregs may thus serve as a fundamental immunotherapy to treat hypertension and CVDs. However, the precise molecular mechanisms underlying the Tregs-induced protection against hypertension and CVDs remain to be investigated. This review focuses on recent advances in our understanding of Tregs subsets and function in CVDs. In addition, we discuss promising strategies for using Tregs through various pharmacological approaches to treat hypertension and CVDs.

Prolonged confinement in cramped spaces can lead to derangements in brain function/structure, yet the underlying mechanisms remain unclear. To investigate, we subjected mice to restraint stress to simulate long-term narrow and enclosed space confinement, assessing their mental state through behavioral tests. Stressed mice showed reduced center travel and dwell time in the Open Field Test and increased immobility in the Tail Suspension Test. We measured lower hippocampal brain-derived neurotrophic factor levels and cortical monoamine neurotransmitters (5-HT and NE) in the stressed group. Further examination of the body\'s immune levels and serum metabolism revealed immune dysregulation and metabolic imbalance in the stressed group. The results of the metabolic network regulation analysis indicate that the targets affected by these differential metabolites are involved in several metabolic pathways that the metabolites themselves participate in, such as the \"long-term depression\" and \"purine metabolism\" pathways. Additionally, these targets are also associated with numerous immune-related pathways, such as the TNF, NF-κB, and IL-17 signaling pathways, and these findings were validated using GEO dataset analysis. Molecular docking results suggest that differential metabolites may regulate specific immune factors such as TNF-α, IL-1β, and IL-6, and these results were confirmed in experiments. Our research findings suggest that long-term exposure to confined and narrow spaces can lead to the development of psychopathologies, possibly mediated by immune system dysregulation and metabolic disruption.

Cancer-associated cachexia (CAC) is a debilitating condition marked by muscle and fat loss, that is unresponsive to nutritional support and contributes significantly to morbidity and mortality in patients with cancer. Immune dysfunction, driven by cytokine imbalance, contributes to CAC progression. This review explores the potential relationship between CAC and anti-cancer immune response in pre-clinical and clinical studies. Pre-clinical studies showcase the involvement of cytokines like IL-1β, IL-6, IL-8, IFN-γ, TNF-α, and TGF-β, in CAC. IL-6 and TNF-α, interacting with muscle and adipose tissues, induce wasting through JAK/STAT and NF-κB pathways. Myeloid-derived suppressor cells (MDSCs) exacerbate CAC by promoting inflammation. Clinical studies confirm elevated pro-inflammatory cytokines (IL-6, IL-8, TNFα) and immune markers like the neutrophil-to-lymphocyte ratio (NLR) in patients with CAC. Thus, immunomodulatory mechanisms involved in CAC may impact the anti-neoplastic immune response. Inhibiting CAC mechanisms could enhance anti-cancer therapies, notably immunotherapy. R-ketorolac, a new immunomodulator, reversed the weight loss and increased survival in mice. Combining these agents with immunotherapy may benefit patients with cancer experiencing CAC. Further research is vital to understand the complex interplay between tumor-induced immune dysregulation and CAC during immunotherapy.

The post-translational modifications (PTMs) of proteins play a crucial role in increasing the functional diversity of proteins and are associated with the pathogenesis of various diseases. This review focuses on a less explored PTM called citrullination, which involves the conversion of arginine to citrulline. This process is catalyzed by peptidyl arginine deiminases (PADs). Different members of the PAD family have distinct tissue distribution patterns and functions. Citrullination is a post-translational modification of native proteins that can alter their structure and convert them into autoantigens; thus, it mediates the occurrence of autoimmune diseases. CD4+ T cells, including Th1, Th2, and Th17 cells, are important immune cells involved in mediating autoimmune diseases, allergic reactions, and tumor immunity. PADs can induce citrullination in CD4+ T cells, suggesting a role for citrullination in CD4+ T cell subset differentiation and function. Understanding the role of citrullination in CD4+ T cells may provide insights into immune-related diseases and inflammatory processes.

BACKGROUND: People who are immune-deficient/disordered (IDP) are underrepresented in COVID-19 studies. Specifically, there is limited research on post-SARS-CoV-2 infection outcomes, including viral persistence and long-term sequelae in these populations.
OBJECTIVE: This review aimed to examine the published literature on the occurrence of persistent SARS-CoV-2 positivity, relapse, reinfections, variant coinfection, and post-acute sequelae of COVID-19 in IDP. Although the available literature largely centred on those with secondary immunodeficiencies, studies on people with inborn errors of immunity are also included.
METHODS: PubMed was searched using medical subject headings terms to identify relevant articles from the last 4 years. Articles on primary and secondary immunodeficiencies were chosen, and a special emphasis was placed on including articles that studied people with inborn errors of immunity. The absence of extensive cohort studies including these individuals has limited most articles in this review to case reports, whereas the articles focusing on secondary immunodeficiencies include larger cohort, case-control, and cross-sectional studies. Articles focusing solely on HIV/AIDS were excluded.
BACKGROUND: Scientific literature suggests that IDP of any age are more likely to experience persistent SARS-CoV-2 infections. Although adult IDP exhibits a higher rate of post-acute sequelae of COVID-19, milder COVID-19 infections in children may reduce their risk of experiencing post-acute sequelae of COVID-19. Reinfections and coinfections may occur at a slightly higher rate in IDP than in the general population.
CONCLUSIONS: Although IDP experience increased viral persistence and inter-host evolution, it is unlikely that enough evidence can be generated at the population-level to support or refute the hypothesis that infections in IDP are significantly more likely to result in variants of concern than infections in the general population. Additional research on the relationship between viral persistence and the rate of long-term sequelae in IDP could inform the understanding of the immune response to SARS-CoV-2 in IDP and the general population.

Coronavirus Disease 2019 (COVID-19) is generally susceptible to the population, highly infectious, rapidly transmitted, and highly fatal. There is a lack of specific drugs against the virus at present and vaccination is the most effective strategy to prevent infection. However, studies have found that some groups, particularly patients with diabetes, show varying degrees of weak immune reactivity to various COVID-19 vaccines, resulting in poor preventive efficacy against the novel coronavirus in patients with diabetes. Therefore, in this study, patients with type 2 diabetes mellitus (T2DM) who had weak immune response to the COVID-19 vaccine in recent years were analyzed. This article reviews the phenomenon, preliminary mechanism, and related factors affecting weak vaccine response in patients with T2DM, which is expected to help in the development of new vaccines for high-risk groups for COVID-19.

Immunoglobulin G4-related disease (IgG4-RD) is a systemic condition known to affect multiple organ systems. While its manifestations are diverse, pulmonary involvement, especially of the pleura, remains less common. We report the case of a 99-year-old Saudi male with a medical history of diabetes mellitus, chronic kidney disease, and hypertension. He presented with dyspnea and syncope, with radiological findings revealing pleural effusion and a mass in the right hemidiaphragm. Laboratory investigations highlighted elevated serum IgG4 levels, and histopathological evaluation confirmed the diagnosis of IgG4-RD. Notably, the patient\'s thoracic histopathology differed from typical IgG4-RD presentations, emphasizing the variability of the disease. This case underscores the significance of recognizing IgG4-RD as a potential cause of unexplained pleural effusion. It also highlights the need for a comprehensive diagnostic approach, integrating laboratory values, histopathological findings, and clinical context. Given the potential variability in thoracic IgG4-RD histopathology, clinicians should maintain a heightened awareness of this condition to avoid missed diagnoses.

CD147/Basigin, a transmembrane glycoprotein belonging to the immunoglobulin superfamily, is a multifunctional molecule with various binding partners. CD147 binds to monocarboxylate transporters (MCTs) and supports their expression on plasma membranes. MTC-1 and MCT-4 export the lactic acid that is converted from pyruvate in glycolysis to maintain the intracellular pH level and a stable metabolic state. Under physiological conditions, cellular energy production is induced by mitochondrial oxidative phosphorylation. Glycolysis usually occurs under anaerobic conditions, whereas cancer cells depend on glycolysis under aerobic conditions. T cells also require glycolysis for differentiation, proliferation, and activation. Human malignant melanoma cells expressed higher levels of MCT-1 and MCT-4, co-localized with CD147 on the plasma membrane, and showed an increased glycolysis rate compared to normal human melanocytes. CD147 silencing by siRNA abrogated MCT-1 and MCT-4 membrane expression and disrupted glycolysis, inhibiting cancer cell activity. Furthermore, CD147 is involved in psoriasis. MCT-1 was absent on CD4+ T cells in CD147-deficient mice. The naïve CD4+ T cells from CD147-deficient mice exhibited a low capacity to differentiate into Th17 cells. Imiquimod-induced skin inflammation was significantly milder in the CD147-deficient mice than in the wild-type mice. Overall, CD147/Basigin is involved in the development of malignant tumors and T-cell-mediated immunological disorders via glycolysis regulation.

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