Measles virus (Morbillivirus abbreviated as MV, but more recently MeV) is the causal agent of measles disease, thought to have existed at least 4,000 years ago, affecting predominantly infants, but also immunocompromised individuals remaining a public health issue today globally. In this review, we discuss the historical background about MeV infection to modern-day research on measles disease, current epidemiology, but also what is known about immunisation against it. We report what is known about the viral structure and the function of the viral proteins. This additionally covers the cellular structure of MeV, mechanisms, and clinical aspects of infection. Including a review of topics like cellular receptor-associated entry factors, to the immunology of MeV infection. In this review, the current knowledge of innate immune responses during infection is explained, which involves changes to chemokine and cytokine expression, finalised by the present understanding of adaptive immune responses to MeV. The genomic stability of the MeV proteins is explained and suggestive that it could be the third pathogen with eradication potential (after the variola and rinderpest viruses). Further biological and immunological clarification as to how this could occur is explained below.

The narrative review aims to shed light on the influence of inflammation in the comorbid chronic pain and major depressive disorder (MDD). This connection is known to be multifactorial, with a dynamic interaction between genetic and epigenetic factors. However, a growing body of evidence has shown that the co-presence of MDD and pain is underlain by immune mechanisms involved in the persistence of the inflammatory process. In particular, the cytokines released following activation of the innate immune system during inflammation cause changes at the endocrine level that result in glucocorticoid resistance, as well as altering the synthesis and metabolism of some central nervous system (CNS) mediators. Cytokines appear to generate neuroinflammation by activating normally protective microglia. Various other mechanisms, including changes in the function of the glutamatergic, GABAergic, and serotonergic systems are also implicated, but inflammation-induced reduction of BDNF (brain-derived neurotrophic factor) appears to be the deciding factor. In turn, neuroinflammation leads to sickness behavior, which is characterized by anhedonia and social withdrawal. This review explored these mechanisms, which may be at the root of comorbid pain and MDD. Although intriguing, however, most available evidence comes from animal studies, and rigorous clinical exploration is warranted.

Atopic dermatitis (AD) is characterized by skin barrier disruption, type 2 immune dysregulation, chronic pruritus, and abnormal colonization by Staphylococcus aureus (S. aureus). Tapinarof, an aryl hydrocarbon receptor modulator, has been demonstrated to attenuate the development of AD in clinical studies. Recently, we found that tapinarof upregulated the expression of filaggrin and loricrin, which are essential proteins in skin barrier functions. Paradoxically, tapinarof induced interleukin (IL)-24 secretion by normal human keratinocytes. IL-24 is produced by T helper 2 lymphocytes and keratinocytes following stimulation by type 2 cytokines, and IL-24 is upregulated in the skin of patients with AD. Furthermore, IL-24 contributes to skin barrier disruption and hyperplasia in AD, and it may exacerbate skin inflammatory responses, itch, andS. aureus infection. In this review, we summarized the current findings regarding the detrimental role of IL-24 in AD, thereby suggesting that co-treatment of tapinarof with therapeutics that block IL-24 signaling may represent a promising strategy for managing AD.

The complement system is a key component of the innate immune system that mediates the clearance of pathogens, apoptotic cells, and cellular debris. However, the complement system also has diverse roles in the central nervous system (CNS), where it regulates synaptic pruning, neural plasticity, and neuroinflammation. Dysregulation of the complement system has been implicated in various neurodegenerative disorders such as Alzheimer’s disease, multiple sclerosis, epilepsy, stroke, and traumatic brain injury. In these conditions, excessive or chronic activation of the complement system may lead to synaptic loss, neuronal damage, immune dysregulation, and inflammation, which leads to exacerbating the disease’s progression and severity. Moreover, the complement system may interact with infectious agents that invade the CNS, such as bacteria, viruses, fungi, and parasites, and modulate their pathogenicity and host response. Therefore, understanding the complex interplay between the complement system and the CNS is crucial for developing novel therapeutic strategies to prevent or treat neurodegenerative and neuroimmune disorders. Natural compounds, such as plant extracts, phytochemicals, and nutraceuticals, have emerged as promising candidates for modulating the complement system and its effects on the CNS. These compounds may exert anti-inflammatory, antioxidant, neuroprotective, and immunomodulatory effects by regulating the expression of various complement components and pathways. In this review, we summarized the current knowledge on the roles of the complement system in human neurodegenerative disorders and the benefits of natural compounds for complement-targeted therapy.

Immunotherapy, a primary anti-neoplastic treatment, exploits the patient’s immune system to kill neoplastic cells by modulating immune checkpoints such as cytotoxic T-lymphocyte antigen 4 and programmed cell death 1. Despite an apparent anti-neoplastic efficacy, immunotherapeutic agents are often accompanied by multiorgan toxicity, including gastrointestinal ones. This particular class of immunotherapy-related adverse events, mainly represented by diarrhea and colitis, necessitates a nuanced treatment strategy. Current treatments are primarily based on standardized severity grading systems to guide and proportion therapeutic interventions, ranging from simple behavioral modifications or conventional molecules (such as anti-diarrheal) to advanced biological treatments. Tofacitinib, a pan-Janus kinase inhibitor, emerged as a potential option for managing immune-related (IR) colitis by targeting hyperactivated T cells within the colic microenvironment. However, evidence supporting the use of tofacitinib in IR colitis is primarily derived from case reports and small case series, lacking robust randomized clinical trial data. While preliminary findings demonstrate encouraging clinical control of IR colitis with tofacitinib, further research is warranted to elucidate its efficacy, safety, optimal dosage, and treatment duration. Although there are some worries about its effects on cancer response and safety, current evidence indicates that tofacitinib could be seen as a possible treatment choice if other therapies with more robust evidence profiles have not been successful.

The tripartite network, including the nervous, immune, and endocrine systems, plays a significant role in regulatory and effector processes in the male body. On the one hand, males perform their reproduction function by generating spermatozoa in conditions of self-tolerance maintenance because most spermatozoa antigens (“sequestrated antigens”) are unknown to the immune system. On the other hand, in everyday life, a male body encounters hostile external infections, some of which colonize the skin and barrier surfaces and present a cancer threat to male genital tracts. This is human papillomavirus (HPV), the “silent killer”. Therefore, the male immune system has to function in a contradictory situation using either active immune responses, self-tolerance mechanisms, or both simultaneously. This review focused on the functional organization of the male immune system, including its coordination with the nervous and endocrine systems, and immune processes at the level of the whole organism, as well as on obvious changes, which have currently happened. The male immune system should function in conditions of the strong influence of testosterone and biosocial impulses coming from the nervous system. In the last century, researchers obtained data showing a decrease in the male reproduction function because of a stable negative dynamic of spermatozoa count and quality. Nowadays, depressing statistical indicators of male fertility have been published. 15% of couples are unable to conceive a child, where 50% of the causes of infertility relate to males, and up to 15% of male infertility cases are due to immunological disorders. It can be assumed that the male immune system starts to function when self-tolerance is partially lost, and the previous balance has been destroyed. Furthermore, sperm allergy has become a new topic in male immunology.

Aim: Hashimoto’s thyroiditis is a polygenic auto-immune disease with a complex etiopathogenesis. It is more common in females. An imbalance between pro-inflammatory and anti-inflammatory cytokines may play an important role in the disease pathogenesis. Numerous studies have been conducted to find an association between genetic polymorphisms and the development of Hashimoto’s thyroiditis. In this context, we proposed to study the impact of the interleukin-6 ( IL-6) gene polymorphism ( rs1800795) on the genetic susceptibility to Hashimoto’s thyroiditis.

Methods: Polymorphism in IL-6 gene ( rs1800795) was assessed in a case-control study involving a population of Western Algeria with 81 Hashimoto’s thyroiditis patients and 211 unrelated healthy subjects, matched in age and sex. The DNA was extracted by a magnetic bead-based technique. The genetic study was performed by molecular biology: real-time PCR using TaqMan single nucleotide polymorphism (SNP) genotyping assay with Applied Biosystems 7500 device.

Results: Results showed that the GG and GC genotypic distribution is similar between patient and control groups with a higher frequency of the GG genotype (80.25% in patients and 78.67% in controls vs. 19.75% of patients and 20.38% of controls with the GC genotype). The CC genotype is absent in patients and present in only 02/211 healthy subjects. The frequency of the polymorphic G allele was similar in the two groups, with 90.1% and 88.8% in patients and controls respectively ( P > 0.05).

Conclusions: This study reports no significant difference in IL-6 ( -174 G/C) gene polymorphism at the allelic or the genotypic level between Hashimoto’s patients and the control group ( P > 0.05). No association between the SNP IL-6 rs1800795 and susceptibility to Hashimoto’s thyroiditis in Western Algerian population.

Cancer-related pain represents one of the most common complaints of cancer patients especially for those with advanced-stage of disease and/or bone metastases. More effective therapeutic strategies are needed not only to improve the survival of cancer patients but also to relieve cancer-related pain. In the last decade, immune checkpoint inhibitor (ICI)-based immunotherapy targeting programmed cell death-1 (PD-1) and its ligand 1 (PD-L1) has revolutionized cancer care. Beyond its anticancer role, PD-1/PD-L1 axis pathway is involved in many other physiological processes. PD-L1 expression is found in both malignant tissues and normal tissues including the dorsal root ganglion, and spinal cord. Through its interaction with PD-1, PD-L1 can modulate neuron excitability, leading to the suppression of inflammatory, neuropathic, and bone cancer pain. Therefore, since the intricate relationship between immunotherapy and pain should be largely dissected, this comprehensive review explores the complex relationship between PD-1/PD-L1-based immunotherapy and cancer-related pain. It delves into the potential mechanisms through which PD-1/PD-L1 immunotherapy might modulate pain pathways, including neuroinflammation, neuromodulation, opioid mechanisms, and bone processes. Understanding these mechanisms is crucial for developing future research directions in order to optimize pain management strategies in cancer patients. Finally, this article discusses the role of artificial intelligence (AI) in advancing research and clinical practice in this context. AI-based strategies, such as analyzing large datasets and creating predictive models, can identify patterns and correlations between PD-1/PD-L1 immunotherapy and pain. These tools can assist healthcare providers in tailoring treatment plans and pain management strategies to individual patients, ultimately improving outcomes and quality of life for those undergoing PD-1/PD-L1-based immunotherapy.

Aim: The immune system can experience temporary suppression following acute or prolonged strenuous exercise, potentially increasing susceptibility to infections. Young athletes, who must balance school, training, studies, and social life, may further disrupt their immune-inflammatory responses. This study aimed to investigate the effects of an 8-week pre-season training on circulating leukocyte responses in well-trained adolescent soccer-players at different stages of puberty.

Methods: Thirty-six soccer players, divided into two groups based on their biological age-under sixteen (U16) and above sixteen (A16)-underwent two rounds of assessments. These included evaluations of anthropometrics, physical fitness, and immune parameters before and after an 8-week pre-season soccer training program.

Results: No significant treatment or interaction effects were found for erythrocyte sedimentation rate (ESR), platelets, total leucocyte count, immune inflammation markers (IIM), weekly rating of perceived exertion, body composition, sit-and-reach flexibility, or VO_2max (P > 0.05). However, post-intervention neutrophil counts were increased, while lymphocyte counts decreased, and IIM levels rose in both groups ( P < 0.05). Neuromuscular explosiveness and strength endurance were significantly higher in the A16 group compared to the U16 group ( P < 0.05). Body fat was reduced, and all physical fitness parameters improved in both groups over time ( P < 0.05).

Conclusions: The 8-week soccer-specific training program did not lead to different effects on immune-inflammatory parameters between youth soccer players at different stages of puberty. However, training adaptations, including improvements in physical fitness, were observed in both groups. This suggests that when the same training load (frequency, duration, intensity) is applied to adolescents at different stages of puberty, immune-inflammatory responses are not significantly influenced by age, but physical fitness improves regardless of puberty stage. A key limitation of this study is the lack analysis of lymphocyte subpopulations, which could provide a deeper understanding of the cellular effects of training on immune function.

The efficacy of chimeric antigen receptor (CAR)-T therapy may not match initial expectations due to the influence of multiple circumstances, some of which cannot be predicted. CAR-T treatment groups include high-risk patients, particularly those with TP53 mutations. A significant body of research has demonstrated that mutations in the TP53 gene play a pivotal role in cancer development and progression. Any aberration in the TP53 gene in cancer is invariably associated with complications and a poor prognosis. Moreover, mutations in the TP53 gene have been observed to correlate with resistance to conventional chemotherapy, prompting the use of alternative therapeutic approaches, including CAR-T therapy. However, there is a possibility that abnormalities in the TP53 gene may affect patients after CAR-T cell administration reducing the efficacy of therapy. This review examines the link between TP53 mutations in cancer and the efficacy of CAR-T therapy, as well as the potential implications of this aspect in therapeutic planning.

Ovarian cancer is the deadliest malignant tumor in the female reproductive system. Despite advancements in standard treatments such as tumor debulking surgery and platinum-based chemotherapy, the overall survival rate remains low. The emergence of targeted therapies, including Poly(ADP-ribose) polymerase (PARP) inhibitors and anti-angiogenic agents, has provided new avenues for treatment. However, drug resistance and disease heterogeneity continue to pose significant challenges. Immune checkpoint inhibitors (ICIs), as an emerging therapeutic approach, primarily target the programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) and cytotoxic T-lymphocyte antigen 4 (CTLA-4) pathways to restore anti-tumor immune responses. Although ICIs have shown significant efficacy in other malignancies, their effectiveness in ovarian cancer is limited, with a response rate of only 10–15% for monotherapy. Recent studies have focused on combining ICIs with chemotherapy, anti-angiogenic agents, or PARP inhibitors to enhance therapeutic outcomes. This article reviews the progress of ICIs in ovarian cancer, including monotherapy and combination treatment strategies, and explores emerging therapeutic targets and strategies aimed at improving patient prognosis and achieving personalized treatment. By gaining a deeper understanding of the tumor microenvironment and its immune evasion mechanisms, there is hope for developing more effective treatment options in the future, ultimately improving the survival rates and quality of life for ovarian cancer patients.