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  • A correlation analysis was performed to investigate a possib

    2023-09-18

    A correlation analysis was performed to investigate a possible relationship between serum resistin levels and MG-ADL. We observed a significant relationship between serum resistin levels and MG-ADL scores in AChR-GMG-positive cases (r=0.285, p=0.032; Fig. 1C). There were also significant correlations between serum resistin levels and MG-ADL scores in patients with thymoma (r=0.453, p=0.014; Fig. 1D). Moreover, no significant correlations were found between the serum resistin levels and anti-AChR antibody scores in patients with anti-AChR antibody-positive MG (r=0.136; p=0.189). We measured serum resistin levels before and after treatment in 6 patients with GMG. We found that serum resistin levels were lower in patients after treatment than in patients not receiving therapy (p=0.031, Fig. 1E).
    Discussion Until now, the role of resistin in MG has been unclear. However, a role for resistin as a proinflammatory cytokine has been demonstrated in several autoimmune diseases. An experimental study in an animal model of rheumatoid arthritis (RA) has shown that recombinant resistin injected into healthy mouse joints can induce infiltration of the synovial tissue by leukocytes, as is observed in the pathology of RA (Bokarewa et al., 2005). Moreover, it has been reported that increased resistin levels in synovial fluid are associated with inflammatory disease. Serum resistin levels are correlated with disease activity and levels of acute phase proteins, including reactive protein and IL-1β. Together, these observations suggest that resistin may be an important mediator of the inflammatory process of RA (Forsblad d'Elia et al., 2008, Schaffler et al., 2003, Senolt et al., 2007). Resistin levels are also associated with lymphocytic inflammation in the salivary glands of patients with primary Sjogren's syndrome (Bostrom et al., 2008). MG is also an autoimmune disorder, primarily caused by autoantibodies against AChR, the production of which depends upon the activation CD4+ T hcv virus and B cells, as well as cytokines. Therefore, resistin may play a similar role in patients with MG. Despite considerable studies concerning resistin pathophysiology, its role in the process of inflammation remains poorly understood. Current evidence indicates that resistin in the form of a peptide hormone is expressed and released by leukocytes, and upregulates the expression of various cytokines such as IL-1, IL-6 and TNF-α via the NF-κB pathway. Resistin itself is increased in leukocytes in response to proinflammatory mediators such as TNF-α, IL-1β, IL-6, or lipopolysaccharide (LPS), suggesting that resistin can enhance its own activity through a positive feedback mechanism (Nagaev et al., 2006, Patel et al., 2003). Considering the involvement of IL-6 and TNF-α in the pathogenesis and immunoregulation of MG (Deng et al., 2002, Duan et al., 2002, Jelinek and Lipsky, 1987), interactions between these molecules and resistin may be important for the inflammatory processes underlying MG pathogenesis. In addition, resistin exerts chemotactic activity on CD4-positive lymphocytes (Walcher et al., 2010). In summary, the ability of resistin to induce pro-inflammatory cytokine expression and release and chemotaxis of CD4-positive lymphocytes suggests that it may play a critical role in MG pathogenesis. Interestingly, high levels of high mobility group box 1 (HMGB1) have been found in several autoimmune diseases such as NMO and MG (Uzawa et al., 2013, Uzawa et al., 2014b). HMGB1 is recognized to be not only a DNA–binding protein, but also a damage associated molecular pattern molecule (DAMP). As a pro-inflammatory mediator, HMGB1 is released from LPS-, TNF a- and IL-1-activated monocytes and macrophages and from other cell types and then acts as an inflammatory trigger and is involved in many inflammatory processes, including cytokine production and B-cell activation. Thus resistin apparently functions by very similar and perhaps cooperative mechanisms to HMGB1 in MG pathogenesis.