Interleukin (IL)-4 and IL-13 belong to the T helper 2 (Th2) cytokine family, along with IL-3, IL-5, and IL-9. These cytokines are key mediators of allergic inflammation. They have important immunomodulatory activities and exert influence on a wide variety of immune cells, such as B cells, eosinophils, basophils, monocytes, fibroblasts, endothelial cells, airway epithelial cells, smooth muscle cells, and keratinocytes. Recent studies have implicated IL-4 and IL-13 in the development of various autoimmune diseases. Additionally, these cytokines have emerged as potential players in pathogenesis of inflammatory arthritis. Recent findings suggest that the IL-4 and IL-13 might play a significant role in the downregulation of inflammatory processes underlying RA pathology, and beneficially modulate the course of the disease. This review summarizes the biological features of the IL-4 and IL-13 and provides current knowledge regarding the role of these cytokines in inflammatory arthritis.

Gamma delta (γδ) T cells represent a unique and distinct population of lymphocytes that bridge the innate and adaptive immune responses. This functional duality positions them as one of the pivotal elements in the evolution and development of the human body’s defense mechanisms. This review aims to provide a comprehensive and in-depth overview of γδ T cells, covering their origins, development, classification, and functional roles in immunology. Special attention is given to their involvement in the pathogenesis of autoimmune and cancer-related diseases—areas that remain subjects of intensive research with many unanswered questions. Additionally, this article explores the therapeutic potential of γδ T cells, which hold promise as a novel approach to treating various difficult-to-manage diseases. The review also presents an analysis of the latest clinical studies utilizing γδ T cells, emphasizing their emerging role in modern medicine. The ultimate goal of this work is to offer a holistic perspective on the current state of research on γδ T cells and their prospective applications in immunotherapy and cancer treatment, highlighting their potential to become a groundbreaking tool in future medical interventions.

Ankylosing spondylitis (AS) is an inflammatory disease that belongs to the spondyloarthritis family. IL-5 and IL-9 belong to the group of Th2 cytokines of anti-inflammatory nature. Polymorphisms in their coding genes have been so far associated with various inflammatory diseases, but there are no reports regarding their involvement in AS pathogenesis to date. The purpose of the study was to investigate relationships between IL5 and IL9 genetic variants with AS susceptibility, clinical parameters as well as response to therapy with TNF inhibitors. In total 170 patients receiving anti-TNF therapy and 218 healthy controls were enrolled in the study. The genotyping of IL5 rs2069812 (A > G) and IL9 rs2069885 (G > A) single nucleotide polymorphisms was performed using the Real-Time PCR method based on LightSNiP kits assays. The present study demonstrated significant relationships between IL5 rs2069812 and IL9 rs2069885 polymorphisms and response to anti-TNF therapy. Presence of the IL5 rs2069812 A allele in patients positively correlated with better response to treatment (p = 0.022). With regard to IL9 rs2069885, patients carrying the A allele displayed better outcomes in anti-TNF therapy (p = 0.046). In addition, IL5 rs2069812 A and IL9 rs2069885 A alleles were associated with lower CRP and VAS values. The obtained results may indicate a significant role for IL-5 and IL-9 in the course of AS and response to anti-TNF therapy.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. While conventional αβ T cells have been extensively studied, the contribution of γδ T cells to RA pathogenesis remains insufficiently understood. Unlike αβ T cells, γδ T cells recognize antigens independently of major histocompatibility complex (MHC) restriction, and their surface receptor expression plays a pivotal role in regulating effector functions. This study aimed to investigate the phenotype and surface receptor profile of γδ T cells in RA patients undergoing anti-TNF therapy, to better understand their potential immunoregulatory and prognostic significance. Peripheral blood samples were collected from RA patients before and during treatment with TNF inhibitors, as well as from healthy controls. Flow cytometry was used to quantify γδ T cell frequency and to assess the expression of selected activation, differentiation, and exhaustion markers on their surface. RA patients exhibited a significant reduction in the frequency of circulating γδ T cells compared with healthy controls. Moreover, γδ T cells in RA displayed phenotypic features of advanced differentiation and functional exhaustion, including altered expression of key surface receptors. The observed alterations in γδ T cell phenotype and receptor expression suggest chronic immune activation in RA. These findings highlight the potential of γδ T cell surface markers as candidate biomarkers for disease activity and response to anti-TNF therapy.