CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
about
Dual effect of chemokine CCL7/MCP-3 in the development of renal tubulointerstitial fibrosis.Vimentin is a dominant target of in situ humoral immunity in human lupus tubulointerstitial nephritisOverexpression of Heme Oxygenase-1 Prevents Renal Interstitial Inflammation and Fibrosis Induced by Unilateral Ureter Obstruction.Continuous AMD3100 Treatment Worsens Renal Fibrosis through Regulation of Bone Marrow Derived Pro-Angiogenic Cells Homing and T-Cell-Related Inflammation.Alterations in Circulating Immune Cells in Neovascular Age-Related Macular Degeneration.Leptospira Interrogans induces fibrosis in the mouse kidney through Inos-dependent, TLR- and NLR-independent signaling pathways.Unilateral ureteral obstruction: beyond obstruction.Roles of lymphocyte kv1.3-channels in the pathogenesis of renal diseases and novel therapeutic implications of targeting the channels.Links between coagulation, inflammation, regeneration, and fibrosis in kidney pathology.Tubular Dickkopf-3 promotes the development of renal atrophy and fibrosis.Type 2 immunity in tissue repair and fibrosis.Contrasting effects of systemic monocyte/macrophage and CD4+ T cell depletion in a reversible ureteral obstruction mouse model of chronic kidney disease.Effects of silica exposure on the cardiac and renal inflammatory and fibrotic response and the antagonistic role of interleukin-1 beta in C57BL/6 mice.T Helper 2 Cytokine Signaling in Bone Marrow-Derived Fibroblasts: A Target for Renal Fibrosis.Thrombospondin-1 deficiency causes a shift from fibroproliferative to inflammatory kidney disease and delays onset of renal failure.Th1/Th2 polarization in tonsillar lymphocyte form patients with IgA nephropathy.Renal fibrosis: Primacy of the proximal tubule.Renal recruitment of B lymphocytes exacerbates tubulointerstitial fibrosis by promoting monocyte mobilization and infiltration after unilateral ureteral obstruction.Depletion of CD8+ T Cells Exacerbates CD4+ T Cell-Induced Monocyte-to-Fibroblast Transition in Renal Fibrosis.Innate Lymphoid Cells: A Promising New Regulator in Fibrotic Diseases.Sulphite oxidase (SO) - a mitochondrial autoantigen as target for humoral and cellular immune reactions in primary sclerosing cholangitis.Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion
P2860
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P2860
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
description
2012 nî lūn-bûn
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2012年の論文
@ja
2012年学术文章
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2012年学术文章
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2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
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2012年學術文章
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2012年學術文章
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name
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@en
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@nl
type
label
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@en
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@nl
prefLabel
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@en
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@nl
P2093
P2860
P356
P1476
CD4+ T Lymphocytes, especially Th2 cells, contribute to the progress of renal fibrosis.
@en
P2093
Guangchang Pei
Huifang Liang
Sheng Chen
Yueqiang Li
P2860
P304
P356
10.1159/000343283
P577
2012-10-09T00:00:00Z