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• W2963112115 abstract "Dear Editor, Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by numerous autoantibodies and pro-inflammatory cytokines. Available evidence suggests that genetic factors and environmental components may perform significantly in the pathogenesis of SLE. It is notable that cytokine-mediated immunity has been demonstrated to play an important role in the development of SLE as well.1 Recently, we read with great interest the article by Kwon et al, who showed that serum levels of interleukin (IL)-32γ were significantly higher in lupus nephritis (LN) patients than in SLE patients without LN and in healthy volunteers.2 With respect to clinical and laboratory features, expressions of C3 and C4 were down-regulated more in LN patients than in SLE patients without LN. Similarly, levels of C-reactive protein, anti-double-stranded DNA (anti-dsDNA) antibody, SLE Disease Activity Index (SLEDAI) were higher in patients with LN as compared to patients without LN.2 Elevated IL-32γ levels negatively related to C3, C4, but positively related to anti-dsDNA and SLEDAI. Interestingly, serum levels of IL-32γ were related to activity and chronicity indices in LN, and IL-32 expression was increased in renal tissues of LN patients more than in healthy controls.2 These data suggest that IL-32γ may correlate with SLE pathogenesis, especially the development of LN, and IL-32γ may be a disease marker for lupus. To date, several studies have discussed the role of IL-32 in lupus, and evaluated the relationship between IL-32 and lupus. However, the results were inconsistent.3-5 Wang et al showed that plasma IL-32 levels in patients with SLE were significantly lower than that in the healthy controls, and IL-32 gene polymorphism rs28372698 was related to susceptibility to SLE.3 In addition, a study assessed the serum IL-32γ expression in SLE patients, and revealed that SLE patients with detectable IL-32γ had histories of LN, and may relate to active disease activity.4 However, Zhang et al reported that serum levels of IL-32 were not strongly different between matched SLE patients and healthy controls.5 Collectively, the above findings showed that whether IL-32 may be of importance in SLE etiology, especially the development of LN, is still needed to be discussed in the future. For instance, to clearly elucidate the association of IL-32 and lupus, the study may consider IL-32 gene knockout mice to directly reveal the relationship. Moreover, to discuss whether IL-32 can be a disease marker for lupus, especially LN, a specific cohort of patients with pre-clinical disease, early disease and long-standing disease for SLE, which are situations where IL-32 has demonstrated diagnostic or predictive utility, may be useful. This work was supported by grants from the National Natural Science Foundation of China (81701606), Southwest Medical University (2018-ZRQN-008). No conflict of interest exist. Wang-Dong Xu and An-Fang Huang designed the study and reviewed, wrote the paper." @default.
• W2963112115 created "2019-07-30" @default.
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• W2963112115 date "2019-07-01" @default.
• W2963112115 modified "2023-10-16" @default.
• W2963112115 title "Comment on: Interleukin‐32γ: Possible association with the activity and development of nephritis in patients with systemic lupus erythematosus" @default.
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• W2963112115 doi "https://doi.org/10.1111/1756-185x.13608" @default.
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