Evaluation of the Relation Between Serum Interleukins 17, 38, 41, and HLA-B27 Gene Expression in Ankylosing Spondylitis Patients

Ankylosing spondylitis (AS) that is known as radiographic SpA (r-axSpA), is a type of axial spondyloarthritis, characterized by the dual pathology of inflammatory bone erosion and aberrant new bone formation. It is characterized by chronic inflammation affecting the sacroiliac joints and spine, leading over time to structural changes such as syndesmophyte formation and spinal ankylosis, with consequent impairment in function and quality of life. As an autoimmune disease, it may also affect several organs, including the eyes, intestines, heart, and lungs .

The global prevalence of AS ranges from 0.3 % to 1.4 %, with a strong predilection for young adult males, in whom mobility and quality of life are often severely impaired. Reports indicate that the global incidence of AS ranges from 0.07 to 0.32%, with a male prevalence 2-3 times higher than that of females .

The etiopathogenesis of spondylo-arthritis is still not fully understood but it has been described as involving several mechanisms of action that synergistically initiate and maintain a pro-inflammatory state, leading to disease onset . Numerous disciplines, including genetics, environment, gut microbiota, and hormones, have previously been studied in relation to the etiology of AS .

Genetic predisposition - particularly carriage of the Human Leukocyte Antigen B27 (HLA-B27) allele - is closely linked to AS susceptibility and underlies several immunopathogenic hallmarks of the disease. There is a growing interest in HLA-B27-based effects, particularly in HLA-B27(+) patients who have AS, although the diagnostic and prognostic functions of HLA-B27 in AS are still being contested. Patients with HLA-B27 positivity have a considerably younger age at onset, a greater number of cases of uveitis, and a higher frequency of involvement of peripheral joints compared to patients with HLA-B27 negative.

The development of inflammatory arthritis is dependent upon the presence of an unbalanced cytokine network. Several interleukins and chemokines, particularly those with pro-inflammatory effects such as tumor necrosis factor (TNF)-α, interleukin (IL)-17A and C-X-C motif chemokine ligand 10 (CXCL10), are involved in mediating inflammation and consequent tissue damage.