NEW! RJR has announced the annually National Award for "Science and Research" for the best scientific articles published throughout the year in the official journal.
Read the Recommendations for the Conduct, Reporting, Editing, and Publication of Scholarly work in Medical Journals.
The published medical research literature is a global public good. Medical journal editors have a social responsibility to promote global health by publishing, whenever possible, research that furthers health worldwide.
INTERLEUKIN (IL) 12, IL-23 AND IL-23 RECEPTOR IN ANKYLOSING SPONDYLITIS PATHOPHYSIOLOGY
Ankylosing spondylitis (AS) is a chronic inflammatory arthritis which involves mainly the spine and the sacroiliac joints, but also the peripheral joints and nonarticular structures. IL-12 and IL-23 are heterodimeric cytokines sharing a common p40 subunit. Studies showed than IL-12 is essential for Th1 differentiation while IL-23 promotes a particular subset of T cells characterized by IL-17 production, called Th17. Since the association of IL-23R with AS was reported, the scientific interest has focused on identifying new single nucleotide polymorphisms (SNPs), present in the coding genes for IL-12/IL-23 subunits and their receptors, that increase the susceptibility for AS. Another point of interest for researchers was to investigate if the identified gene variants modify the gene expression of the respective interleukins and/or their receptors, whether that refers to their mRNA expression, their serum levels or the expression of the receptors on the surface of T cells. Given the increasing amount of data that suggests the pivotal role of the IL-23/Th17 axis in AS pathophysiology, new promising therapies, designed to interfere with these pathways, are now in development.
Keywords: IL-12, IL-23, IL-23R, ankylosing spondylitis, single nucleotide polymorphisms (SNPs)