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IFN-γ, should not be ignored in SLE.

ABSTRACT: Systemic lupus erythematosus (SLE) is a typical autoimmune disease with a complex pathogenesis and genetic predisposition. With continued understanding of this disease, it was found that SLE is related to the interferon gene signature. Most studies have emphasized the important role of IFN-α in SLE, but our previous study suggested a nonnegligible role of IFN-γ in SLE. Some scholars previously found that IFN-γ is abnormally elevated as early as before the classification of SLE and before the emergence of autoantibodies and IFN-α. Due to the large overlap between IFN-α and IFN-γ, SLE is mostly characterized by expression of the IFN-α gene after onset. Therefore, the role of IFN-γ in SLE may be underestimated. This article mainly reviews the role of IFN-γ in SLE and focuses on the nonnegligible role of IFN-γ in SLE to gain a more comprehensive understanding of the disease.

SUBMITTER: Liu W

PROVIDER: S-EPMC9399831 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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IFN-γ, should not be ignored in SLE.

Liu Wenping W Zhang Shumin S Wang Jibo J

Frontiers in immunology 20220810

Systemic lupus erythematosus (SLE) is a typical autoimmune disease with a complex pathogenesis and genetic predisposition. With continued understanding of this disease, it was found that SLE is related to the interferon gene signature. Most studies have emphasized the important role of IFN-α in SLE, but our previous study suggested a nonnegligible role of IFN-γ in SLE. Some scholars previously found that IFN-γ is abnormally elevated as early as before the classification of SLE and before the eme ...[more]

PMID: 36032079

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Project description:BackgroundSystemic Lupus Erythematosus (SLE) is characterized by dysregulated immune responses, with neutrophil extracellular traps (NETs) playing a significant role. NETs are recognized by autoantibodies in SLE patients, exacerbating pathology. Both excessive NET formation and impaired degradation contribute to SLE pathophysiology.ObjectiveTo investigate the immunomodulatory effects of Dexamethasone-primed Wharton's jelly (WJ) derived MSCs CM (DW) and IFN-γ-primed WJ-MSCs-CM (IW) on NETosis and associated protein markers in SLE patients' LPS or ribonucleoprotein immune complexes (RNP ICs) induced neutrophils and in pristane induced lupus (PIL) model. And to elucidate the mechanism involved therein.MethodsWe investigated the immunomodulatory effects of DW and IW on NETosis in SLE. Utilizing ex vivo and in vivo models, we assessed the impact of preconditioned media on NET formation and associated protein markers neutrophil elastase (NE), citrullinated histone (citH3), myeloperoxidase (MPO), cytoplasmic and mitochondrial ROS production. We also examined the involvement of key immunomodulatory factors present in DW and IW, including prostaglandin E2 (PGE2), indoleamine 2,3-dioxygenase (IDO), and transforming growth factor-beta (TGF-β).ResultsPreconditioned media effectively suppressed NETosis and reduced ROS generation in SLE neutrophils, indicating their immunomodulatory potential. Inhibition studies implicated IDO and PGE2 in mediating this effect. Combined treatment with DW or IW together with hydroxychloroquine (HCQ) demonstrated superior efficacy over HCQ alone, a standard SLE medication. In PIL mouse model, DW and IW treatments reduced NETosis, ROS generation, as evidenced by decreased NET-associated protein expression in vital organs.ConclusionOur study highlights the multifaceted impact of IW and DW on NETosis, ROS dynamics, and lupus severity in SLE. These findings underscore the potential of preconditioned media for the development of targeted, personalized approaches for SLE treatment.

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IFN-γ, should not be ignored in SLE.

Publications

IFN-γ, should not be ignored in SLE.

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