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Th1 and Th17 cells induce proliferative glomerulonephritis.

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Th1 and Th17 cells induce proliferative glomerulonephritis. / Summers, Shaun A; Steinmetz, Oliver; Li, Ming; Kausman, Joshua Y; Semple, Timothy; Edgtton, Kristy L; Borza, Dorin-Bogdan; Braley, Hal; Holdsworth, Stephen R; Kitching, A Richard.

In: J AM SOC NEPHROL, Vol. 20, No. 12, 12, 2009, p. 2518-2524.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Summers, SA, Steinmetz, O, Li, M, Kausman, JY, Semple, T, Edgtton, KL, Borza, D-B, Braley, H, Holdsworth, SR & Kitching, AR 2009, 'Th1 and Th17 cells induce proliferative glomerulonephritis.', J AM SOC NEPHROL, vol. 20, no. 12, 12, pp. 2518-2524. <http://www.ncbi.nlm.nih.gov/pubmed/19820122?dopt=Citation>

APA

Summers, S. A., Steinmetz, O., Li, M., Kausman, J. Y., Semple, T., Edgtton, K. L., Borza, D-B., Braley, H., Holdsworth, S. R., & Kitching, A. R. (2009). Th1 and Th17 cells induce proliferative glomerulonephritis. J AM SOC NEPHROL, 20(12), 2518-2524. [12]. http://www.ncbi.nlm.nih.gov/pubmed/19820122?dopt=Citation

Vancouver

Summers SA, Steinmetz O, Li M, Kausman JY, Semple T, Edgtton KL et al. Th1 and Th17 cells induce proliferative glomerulonephritis. J AM SOC NEPHROL. 2009;20(12):2518-2524. 12.

Bibtex

@article{b9f0ecad9ec146828181b7c30a8084cd,
title = "Th1 and Th17 cells induce proliferative glomerulonephritis.",
abstract = "Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.",
author = "Summers, {Shaun A} and Oliver Steinmetz and Ming Li and Kausman, {Joshua Y} and Timothy Semple and Edgtton, {Kristy L} and Dorin-Bogdan Borza and Hal Braley and Holdsworth, {Stephen R} and Kitching, {A Richard}",
year = "2009",
language = "Deutsch",
volume = "20",
pages = "2518--2524",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "12",

}

RIS

TY - JOUR

T1 - Th1 and Th17 cells induce proliferative glomerulonephritis.

AU - Summers, Shaun A

AU - Steinmetz, Oliver

AU - Li, Ming

AU - Kausman, Joshua Y

AU - Semple, Timothy

AU - Edgtton, Kristy L

AU - Borza, Dorin-Bogdan

AU - Braley, Hal

AU - Holdsworth, Stephen R

AU - Kitching, A Richard

PY - 2009

Y1 - 2009

N2 - Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.

AB - Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.

M3 - SCORING: Zeitschriftenaufsatz

VL - 20

SP - 2518

EP - 2524

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 12

M1 - 12

ER -