Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin condition characterized by intense pruritus and a significant impact on a patient’s quality of life. Despite advancements in understanding AD pathophysiology, there remains a critical need for innovative therapeutic options to better manage this debilitating disease. This review focuses on the evolving landscape of biological therapies for AD, offering insights into their role, mechanisms of action, and potential to revolutionize patient care. In this review, we explore the underlying immunological mechanisms of AD, particularly the role of cytokines and immune pathways implicated in the disease, and how targeted biological therapies modulate these pathways. Current FDA- and EMA-approved biologics, such as Dupilumab, are also discussed in terms of their mechanisms of action, efficacy, and safety. Additionally, we compare their effectiveness, highlighting the benefits and limitations observed in clinical practice. Emerging biological therapies currently under development offer new hope, with innovative targets like IL-13, IL-31, and thymic stromal lymphopoietin (TSLP) representing promising avenues for intervention. We also delve into personalized medicine, emphasizing the importance of biomarkers for predicting treatment response and stratifying AD patients to optimize therapeutic outcomes. Moreover, the synergistic potential of combining biologics with traditional therapies is reviewed, along with a discussion of the challenges involved, including safety, long-term efficacy, and patient adherence. We address the future direction of AD treatment, including microbiome-targeting biologics and the development of next-generation immune modulators. We highlight a new era of targeted treatment possibilities for this complex condition.

Cutaneous warts caused by human papillomavirus (HPV) are among the most common dermatological conditions, affecting the quality of life of numerous people. Although they are widespread, effective and reliable treatment alternatives are limited, emphasizing the necessity for novel treatment options. Intralesional immunotherapy has emerged as a promising alternative, aiming to stimulate the host immune response to achieve the clearance of both treated and distant lesions. This review explores the immunopathogenesis of cutaneous warts and provides an in-depth analysis of intralesional therapies including measles–mumps–rubella (MMR) vaccine, purified protein derivative (PPD), Bacillus Calmette–Guérin (BCG), Candida antigen, Mycobacterium w vaccine (MWV), vitamin D3, and autoinoculation. We provide a comprehensive analysis of the most promising modalities, highlighting their mechanism of action, outcomes, advantages, and limitations. Although initial data indicate that intralesional immunotherapy offers advantageous efficacy and tolerability, there is a lack of standardized treatment protocols and randomized controlled trials to endorse its broad application. Nevertheless, considering its potential to address local and distant lesions with minimal adverse effects, intralesional immunotherapy may represent a transformative approach to managing cutaneous warts.

Iron deficiency (ID) has emerged as a pivotal yet underrecognized factor in the pathogenesis of immune-mediated inflammatory skin diseases (IMISDs) such as psoriasis, atopic dermatitis, and hidradenitis suppurativa. Beyond its classical role in erythropoiesis, iron acts as a key modulator of immune cell activity, redox balance, and overall metabolic homeostasis. This review synthesises the latest evidence on the intricate relationship between systemic inflammation, disturbances of iron metabolism, and immunometabolic imbalances that underline the pathogenesis of IMISDs. Findings indicate that chronic inflammation drives functional iron deficiency through IL-6–hepcidin-mediated sequestration of iron, resulting in reduced bioavailability and altered mitochondrial activity in immune and epithelial cells. This imbalance is associated with excessive and chronically enhanced oxidative and inflammatory responses of these cells, further advancing inflammation, anaemia of chronic disease, and disturbances of tissue repair. Moreover, emerging evidence supports an “iron-skin axis,” and suggests that skin cells, particularly epidermal keratinocytes, are actively involved in the regulation of iron pathways. Collectively, these insights position iron homeostasis as a missing link between systemic inflammation, immunometabolic imbalance, and disease burden in IMISDs.

Introduction: Withania Somnifera (Ashwagandha), an ancient ayurvedic remedy, has been valued for centuries in traditional medicine due to its versatility of beneficial properties on the body system. Contemporary research aims to expand the medicinal use of Ashwagandha and fully harness its adaptogenic potential. Recently, Ashwagandha has gained the rising interest of sportsmen seeking effective and natural ways to enhance their performance. Purpose of the work: The aim of this study is to review existing research on the effects of Withania Somnifera (Ashwagandha) supplementation on performance, as well as its beneficial impact on overall health and well-being of athletes. Materials and methods: A comprehensive literature search and analysis was conducted on PubMed, Google Scholar, Scopus and Science Direct databases using combinations of the following phrases: „Withania Somnifera”; „Ashwagandha”; „Adpatogens”; „Health Benefits of Ashwagandha”; „Ashwagandha and Physical Performance”; „Ashwagandha and Endurance”; „Adverse Effects of Ashwagandha”. Results: Supplementation of Ashwagandha has been demonstrated to enhance physical performance and recovery in athletes, as well as significantly improve strength and muscle mass. Furthermore, supplementation provides various health benefits for the body, with emphasis on improved sleep quality and reduced stress and anxiety. Research recognises Ashwagandha as safe and well-tolerated.

Generalized pustular psoriasis (GPP) is a rare, severe, and potentially life-threatening inflammatory dermatosis increasingly recognized as a distinct disease entity rather than a variant of plaque psoriasis. Emerging evidence indicates that GPP is primarily driven by dysregulation of the interleukin-36 (IL-36) signaling axis, leading to amplification of proinflammatory cascades in keratinocytes and a predominantly innate, neutrophil-driven immune response. This promotes rapid neutrophil recruitment, sterile pustule formation, and abrupt cutaneous and systemic inflammation. Consistent with this, GPP demonstrates a greater predominance of innate immune and neutrophil-driven inflammation, whereas plaque psoriasis is more strongly associated with IL-23/Th17-mediated adaptive immune responses. Transcriptomic and genetic studies further support this distinction, demonstrating enrichment of IL-36-associated and neutrophil-related signatures, activation of MyD88-dependent pathways, and mutations in genes regulating the IL-36 axis, including IL36RN, AP1S3, and CARD14. Consequently, conventional systemic therapies and biologics targeting TNF-α, IL-17, and IL-23 pathways show variable efficacy and may act more slowly in GPP. In contrast, IL-36 receptor inhibitors represent a more mechanism-aligned approach and have demonstrated rapid and clinically meaningful responses in acute flares. However, important gaps remain, including the lack of validated biomarkers and limited data on long-term treatment outcomes. This review provides an integrated perspective on IL-36-driven inflammation in GPP, including comparison with plaque psoriasis, and outlines its implications for mechanism-based therapeutic approaches.

High-performance athletes are increasingly exposed to frequent trans-meridian travel, leading to profound circadian desynchronization and gastrointestinal distress. This review examines the complex interplay between the host’s central circadian system and the gut microbiota (GM), both of which exhibit synchronised daily oscillations essential for homeostasis. Rapid time-zone transitions, such as those anticipated for the 2026 FIFA World Cup, induce a state of “gut jet lag,” characterised by the loss of rhythmic microbial functions and impaired intestinal barrier integrity. Circadian misalignment is associated with increased systemic inflammation and disrupted metabolic regulation, which may contribute to impairments in cognitive performance, sleep quality, and muscle recovery. Critically, travel-induced dysbiosis may reduce the production of microbial metabolites, specifically short-chain fatty acids (SCFAs) like acetate, propionate, and butyrate. These SCFAs serve as energy substrates that may enhance glucose uptake, lipid oxidation, and glycogen storage in skeletal muscle. Evidence suggests that travel-related stressors—including dehydration, psychological stress, and shifts toward highly processed diets—further exacerbate the loss of beneficial taxa. To mitigate these effects, this article proposes evidence-informed strategies: timed light exposure to reset the master clock, chronobiotic meal timing to entrain peripheral tissues, and targeted symbiotic supplementation to restore SCFA-producing populations. Integrating these personalised, evidence-informed protocols may support the optimisation of physiological resilience and performance.