Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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наукова стаття, опублікована у 2018

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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P1476

Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion

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P2093

Chunxiu Zhang

http://www.w3.org/2001/XMLSchema#string

Gang Xu

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Haotian Wei

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Kun Wang

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Ran Luo

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Shuwang Ge

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Xinjun Liang

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Yanyan Liu

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Ying Zhang

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Yueqiang Li

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P2860

Type-1 pericytes accumulate after tissue injury and produce collagen in an organ-dependent manner

Macrophage and Innate Lymphoid Cell Interplay in the Genesis of Fibrosis

Pericytes and immune cells contribute to complement activation in tubulointerstitial fibrosis.

IL-17 produced by neutrophils regulates IFN-gamma-mediated neutrophil migration in mouse kidney ischemia-reperfusion injury.

Cellular and molecular mechanisms in kidney fibrosis.

Anti-Double-Stranded DNA IgG Participates in Renal Fibrosis through Suppressing the Suppressor of Cytokine Signaling 1 Signals.

Origin and function of myofibroblasts in kidney fibrosis.

The attenuation of renal fibrosis by histone deacetylase inhibitors is associated with the plasticity of FOXP3+IL-17+ T cells

Tumor microenvironment macrophage inhibitory factor directs the accumulation of interleukin-17-producing tumor-infiltrating lymphocytes and predicts favorable survival in nasopharyngeal carcinoma patients.

Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells.

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2385

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scholarly article

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10.3389/FIMMU.2018.02385

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English

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P577

2018-01-01T00:00:00Z

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30405606

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6204358

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