Association of CD30 transcripts with Th1 responses and proinflammatory cytokines in patients with end-stage renal disease

Velásquez, Sonia Y.; Opelz, Gerhard; Rojas, Mauricio; Süsal, Caner; Álvarez, Cristiam M.

doi:10.1016/j.humimm.2016.03.004

Cited by 1 publication

(1 citation statement)

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“…These cytokines are upregulated in kidneys with inflammation and fibrosis and attract inflammatory cells, such as monocytes, T lymphocytes, and neutrophils [37, 38]. Monitoring of these cytokines may help follow up the progression of renal diseases [39, 40]. Our results showed that the mRNA expression levels of RANTES, MCP-1, and IP-10 were higher in the WT mice when compared with the Fn14-KO mice, both of which received injection of anti-dsDNA IgG hybridoma cells.…”

Section: Discussionmentioning

confidence: 99%

Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice

Min

Wang

et al. 2018

Journal of Immunology Research

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Many studies have demonstrated that anti-dsDNA IgG is closely associated with lupus nephritis. Recently, it was found that activation of the fibroblast growth factor-inducible 14 (Fn14) signaling pathway damages glomerular filtration barrier in MRL/lpr lupus-prone mice. However, MRL/lpr mice have high titers of serum autoantibodies other than anti-dsDNA IgG. The aim of this study was to further explore the effect of Fn14 deficiency on anti-dsDNA IgG-induced glomerular damage in severe combined immunodeficiency (SCID) mice that have no endogenous IgG. Fn14 deficiency was generated in SCID mice. The murine hybridoma cells producing control IgG or anti-dsDNA IgG were intraperitoneally injected into mice. In two weeks, the urine, serum, and kidney tissue samples were harvested from mice at sacrifice. It showed that the injection of anti-dsDNA IgG, but not control IgG hybridoma cells, induced proteinuria and glomerular damage in SCID mice. Between the wild-type (WT) and knockout (KO) mice injected with anti-dsDNA IgG hybridoma cells, the latter showed a decrease in both proteinuria and glomerular IgG deposition. The histopathological changes, inflammatory cell infiltration, and proinflammatory cytokine production were also attenuated in the kidneys of the Fn14-KO mice upon anti-dsDNA IgG injection. Therefore, Fn14 deficiency effectively protects SCID mice from anti-dsDNA IgG-induced glomerular damage.

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