4.5 Review

Role of the innate and adaptive immune responses in the pathogenesis of systemic lupus erythematosus

Journal

INFLAMMATION RESEARCH
Volume 71, Issue 5-6, Pages 537-554

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s00011-022-01554-6

Keywords

Cytokines; Immune cells; Immunopathogenesis; Systemic lupus erythematosus

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Systemic lupus erythematosus (SLE) is a multisystemic rheumatic disease that primarily affects women of childbearing age. The common symptoms of SLE closely resemble those of other autoimmune and non-autoimmune disorders. This article provides an overview of the most up-to-date information on immune system-related factors, cells, and cytokines involved in the pathogenesis of SLE.
Objective Systemic lupus erythematosus (SLE), the most common form of lupus, is a multisystemic rheumatic disease with different clinical features that generally affect women of childbearing age. The common symptoms of SLE are very similar to other autoimmune and non-autoimmune disorders, thereby it is known as a thousand faces disease. In this article, we are going to discuss some of the most updated information about immune system-related factors, cells, and cytokines involved in SLE pathogenesis. Methods Different electronic databases, especially PubMed/MEDLINE, Scopus, and Google Scholar, were searched to review and analyze relevant literature on the role of innate and adaptive immune cells and cytokines in the pathogenesis of SLE. A search for relevant literature was accomplished using various keywords including systemic lupus erythematosus, apoptosis, autoantibodies, immunopathogenesis of SLE, adaptive and innate immune cells, inflammatory cytokines, hormones, etc. Results and conclusion The most important characteristic of SLE is the production of antibodies against different nuclear autoantigens like double-strand DNA and RNA. The depositions of the immune complexes (ICs) that are generated between autoantibodies and autoantigens, along with aberrant clearance of them, can lead to permanent inflammation and contribute to tissue or organ damage. Related mechanisms underlying the initiation and development of SLE have not been clarified yet. Although, defects in immune tolerance, enhanced antigenic load, hyperactivity of T cells, and inappropriate regulation of B cells contribute to the pathogenic autoantibodies generation. Besides, sex hormones that influence the immune system seem to act as triggers or protectors of SLE development.

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