Roles of IL‐1 and IL‐10 family cytokines in the progression of systemic lupus erythematosus: Friends or foes?

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology that can affect nearly every organ system in the body. Besides genetic and environmental factors, unbalanced pro‐inflammatory and anti‐inflammatory cytokines contribute to immune dysregulation, trigger an inflammatory response, and induce tissue and organ damage. Inflammatory responses in SLE can be promoted and/or maintained by the availability of cytokines that are overproduced systemically and/or in local tissues. Several key cytokines have been considered potential targets for the reduction of chronic inflammation in SLE. Recent studies indicated that dysregulated production of several cytokines, including those of the IL‐1 family and IL‐10 family, orchestrate immune activation and self‐tolerance, play critical roles in the pathogenesis of SLE. Among IL‐1 family cytokines, IL‐1, IL‐18, IL‐33, IL‐36, IL‐37, and IL‐38 had been the most thoroughly investigated in SLE. Additionally, IL‐10 family cytokines, IL‐10, IL‐20, IL‐22, IL‐26, IL‐28, and IL‐29 are dysregulated in SLE. Therefore, a better understanding of the initiation and progression of SLE may provide suitable novel targets for therapeutic intervention. In this review, we discuss the involvement of inflammation in the pathogenesis of SLE, with a focus on IL‐1 family and IL‐10 family cytokines, and highlight pathophysiological approaches and therapeutic potential for treating SLE.

Systemic lupus erythematosus variants modulate the function of an enhancer upstream of TNFAIP3

“…IL20RA encodes the alpha subunit of the Interleukin-20 (IL-20) receptor. The IL-20 signaling axis influences the crosstalk between lymphocytes and epithelial cells, including facilitating the infiltration of immune cells to the kidneys in murine lupus nephritis models ( Wu et al, 2022 ). IL-20 signaling also activates proinflammatory responses and reactive oxygen species production that contribute to renal tissue damage.…”

From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review

“…Sickness behavior is associated mostly with acute inflammation in the presence of infection. However, the same cytokines thought to be responsible for this behavioral pattern are present and exert systemic actions in other inflammatory diseases, such as RA, systemic lupus erythematosus (SLE), and OA [96,262,263]. Patients with RA and SLE are known to suffer from fatigue and depressed mood [264,265].…”

The Impact of the IL-10 Gene Polymorphism on mRNA Expression and IL-10 Serum Concentration in Polish Lupus Patients

“…The dysregulation of homeostatic cytokine levels has been implicated in the etiology of autoimmune diseases [7,8]. Recently, a lot of interest has been directed towards interleukin 10 (IL-10) in SLE pathogenesis [9,10]. It plays a key role during innate and adaptive immune responses, because it has a wide variety of functions in T, B, natural killer, and dendritic cells, as well as in macrophages.…”