Abstract
Rheumatoid arthritis (RA) is an autoimmune inflammatory joint disease with complex pathogenesis associated with cytokine dysregulation. Macrophage migration inhibitory factor (MIF) plays a role in systemic inflammation and joint destruction in RA and could be associated with the secretion of other immune-modulatory cytokines such as IL-25, IL-31, and IL-33. For the above, our main aim was to evaluate the IL-25, IL-31, and IL-33 secretion from recombinant human MIF (rhMIF)-stimulated peripheral blood mononuclear cells (PBMC) of RA patients. The rhMIF and lipopolysaccharide (LPS) plus rhMIF stimuli promote the secretion of IL-25, IL-31, and IL-33 (p < 0.05) from PBMC of RA patients. The study groups, the different stimuli, and the interaction between both showed a statistically significant effect on the secretion of IL-25 (p < 0.05) and IL-31 (p < 0.01). The study of the effect of the RA patient treatments and their interaction with the effect of stimuli did not show an interaction between them. In conclusion, our study generates new evidence for the role of MIF in the secretion of IL-25, IL-31, and IL-33 and its immunomodulatory effect on RA.
Highlights
Rheumatoid arthritis (RA) is an autoimmune chronic disease associated with high levels of proinflammatory cytokines, secreted mainly by mononuclear cells such as T lymphocytes and macrophages [1]
It has been shown in a mouse model of collagen-induced arthritis that high expression of IL-25 is related to a regulatory mechanism in the presence of high levels of IL-17 [4], and it has been found that IL-33 can intensify collagen-induced arthritis in experimental models [5]
We have been interested in knowing the cellular response mediated by migration inhibitory factor (MIF) in RA in such a way that we set out to investigate whether there is a relationship between MIF and the production of other cytokines recently related to the pathogenesis of this disease, such as IL-25, IL-31, and IL-33
Summary
Rheumatoid arthritis (RA) is an autoimmune chronic disease associated with high levels of proinflammatory cytokines, secreted mainly by mononuclear cells such as T lymphocytes and macrophages [1]. In macrophages and synovial fibroblasts, MIF induces the expression of tissue-destructive cytokines and mediators, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-8, and some matrix metalloproteinases (MMP) such as MMP-1 and MMP-3 [3]. In addition to MIF, other cytokines such as IL-25, IL-31, and IL-33 are involved in the pathogenesis of different inflammatory diseases, including RA. It has been shown in a mouse model of collagen-induced arthritis that high expression of IL-25 is related to a regulatory mechanism in the presence of high levels of IL-17 [4], and it has been found that IL-33 can intensify collagen-induced arthritis in experimental models [5]. Complementary with this, high levels of IL-25 in the synovial fluid and serum of RA patients have been reported [4] and evidence for the relationship between IL-33 and RA exists, since IL-33 levels are higher in patients compared to healthy subjects [6]
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