Mucosal immunity and trained innate immunity of the gut play a pivotal role in maintaining intestinal homeostasis and defending against microbial pathogens. This review provides an overview of the mechanisms underlying mucosal immunity and the concept of trained innate immunity in the gut. We discuss the interaction between gut microbiota and the host immune system, highlighting the role of epithelial cells, dendritic cells, and innate lymphoid cells, as well as the novel concept of trained innate immunity and its role in perpetuating or attenuating gut inflammation. We also comment on the current models for investigating mucosal immunity, their limitations, and how they can be overcome. Additionally, we explore the potential therapeutic implications of modulating mucosal immunity and trained innate immunity in gastrointestinal diseases. Only by elucidating the mechanisms underlying mucosal immunity and the concept of trained innate immunity, innovative approaches to modulate immune responses and restore intestinal homeostasis in the context of gastrointestinal disorders could be implemented.

Rheumatoid arthritis (RA) is an immune-mediated chronic and long-term condition that can lead to severe joint damage and disability. It has been shown that doctor–patient interaction and communication can have a significant impact on faster patient diagnosis and treatment outcomes. Primary care (PC) is the first level of patient contact with doctors and the health system. Communication between them is often ineffective, leading to delays in diagnosis, care, and the use of disease-modifying antirheumatic drugs (DMARDs). The protocols and standards for the treatment of RA are well established by all rheumatology organizations. All of them recommend early initiation of DMARDs, which leads to better long-term outcomes. There are some recommendations that would lead to better optimization of recognition, management, and referral practices. Early diagnosis, effective communication between general practitioners and specialists, and patient education about possible targeted therapies and biological products, as well as subsequent monitoring of therapies and screening for risk factors and comorbidities, will improve patient health and optimize costs. We aimed to offer strategies and possibilities for integrating and optimizing primary care and specialized therapies in RA because proper management will reduce the severity of the disease and even reduce mortality from chronic diseases such as RA.

In recent years, Meteorin-like protein (Metrnl/IL-41) and Follistatin-like 1 (FSTL1) have emerged as multifunctional molecules that play roles in immunity, metabolism and tissue remodeling. Although they demonstrate pleiotropic effects, they are promising candidates for biomarkers and possible therapeutic targets. The development of new, disease-specific biomarkers will enable clinicians to more effectively monitor inflammatory activity, more accurately assess disease severity, better predict survival, and select appropriate medical treatments. In this review, we present the role of Meteorin-Like Protein (Metrnl) and Follistatin-like 1 (FSTL1) in inflammation in autoimmune rheumatic diseases, as well as in other autoimmune pathologies, cardiovascular diseases, and metabolic diseases. Metrnl, widely expressed in different tissues and organs, is very important for inflammation, immune responses and metabolic disorders. FSTL1 also shows dynamic changes in its expression through various diseases, including cardiovascular conditions, cancer, asthma, and arthritis. Both proteins participate in multiple important signaling pathways, and understanding their diagnostic and therapeutic potential holds great scientific interest. Their complex nature requires careful evaluation of safety concerns and translation to clinical practice.

Systemic necrotising vasculitides (SNVs) pose significant challenges due to their diverse clinical manifestations and variable outcomes. Therefore, identifying reliable biomarkers holds promise for improving precision medicine in SNVs. This review explores emerging biomarkers aiming to enhance diagnostic accuracy, prognostic assessment, and disease monitoring. We discuss recent advances in immunological biomarkers, inflammatory indicators, and other parameters that exhibit potential diagnostic and prognostic utility. A comprehensive understanding of these biomarkers may facilitate earlier and more accurate SNV detection, aiding in timely intervention and personalized treatment strategies. Furthermore, we highlight the evolving landscape of disease monitoring through innovative biomarkers, shedding light on their dynamic roles in reflecting disease activity and treatment response. Integrating these novel biomarkers into clinical practice can revolutionize the management of SNVs, ultimately improving patient outcomes and quality of life.

Coronary artery disease (CAD) presents a significant risk for patients with systemic vasculitides, a group of disorders characterized by the inflammation of blood vessels. In this review, we focus on the pathophysiological mechanisms, complications, and management strategies for CAD in systemic vasculitides. We highlight how the inflammatory processes inherent in vasculitis contribute to accelerated atherosclerosis and myocardial ischemia. Key strategies in managing CAD in this patient population include using medicine treatments to mitigate vascular inflammation while balancing the risk of promoting cardiovascular events and lifestyle modifications. Understanding the nuanced relationship between systemic vasculitides and CAD is crucial for improving patient outcomes and guiding therapeutic approaches.

Background: Systemic sclerosis (SSc) represents a multidimensional disease affecting various organs and systems, with the common denominator being the vascular pathology encountered in the micro- and macrocirculation of SSc patients. Recently, much progress has been made toward understanding the molecular basis of endothelial injury and subsequent fibroblast activation, thus paving the way for specific therapy that can target and counteract these processes. Aim: In this review, we examined the latest preclinical and clinical data on therapeutic options to address vascular abnormalities in SSc. Results: We discuss the efficacy of current treatments, including pharmacological agents and emerging therapies, in mitigating vascular damage and improving patient outcomes based on preclinical models and clinical trials that offer evidence of their safety and effectiveness. Conclusions: Although promising therapeutic strategies emerge, optimizing the management of vascular abnormalities in SSc requires further research.