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Adaptive Immune-Related Cells and Cytokines in Spondyloarthropathies Publisher



Akhtari M1
Authors

Source: Ankylosing Spondylitis - Axial Spondyloarthritis: Cellular# Molecular and Environmental Factors Published:2021


Abstract

Spondyloarthropathies (SpAs) including ankylosing spondylitis (AS), inflammatory bowel disease (IBD) associated arthritis, psoriatic arthritis (PsA), reactive arthritis (ReA), and undifferentiated spondyloarthropathies (uSpAs) are a subset of disorders with strong adaptive and inflammatory innate immunity overlaps. The immunopathology of this group of rheumatic diseases is related to MHC class-I molecule and adaptive immune responses. Adaptive immunity is composed of specialized T and B cell lineage lymphocytes and includes both humoral and cell-mediated immune mechanisms. T lymphocytes are divided into the CD4+ (helper T) and CD8+ (cytotoxic T) cells based on the surface receptors. Based on the secretory cytokines, helper T cells are sorted into Th1, Th2, Th17, Th22, and regulatory T lymphocytes (Treg) and cytotoxic T cells (CTL) are sorted into Tc1, Tc2, and Tc17. A pathogenic role of Th17 and Th22, the defect in the regulatory function of Treg lymphocytes, dysregulated Th1 and Th2 function, aberrant cytotoxicity function of T CD8+, and abnormal B cells activity have been described to be associated with the pathogenesis of SpAs. In this chapter, we discuss recent findings regarding the pathogenic role of adaptive immunity in SpA disorders. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022.
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