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Podocytes use FcRn to clear IgG from the glomerular basement membrane

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Podocytes use FcRn to clear IgG from the glomerular basement membrane. / Akilesh, Shreeram; Huber, Tobias B; Wu, Hui; Wang, Gary; Hartleben, Björn; Kopp, Jeffrey B; Miner, Jeffrey H; Roopenian, Derry C; Unanue, Emil R; Shaw, Andrey S.

in: P NATL ACAD SCI USA, Jahrgang 105, Nr. 3, 22.01.2008, S. 967-72.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Akilesh, S, Huber, TB, Wu, H, Wang, G, Hartleben, B, Kopp, JB, Miner, JH, Roopenian, DC, Unanue, ER & Shaw, AS 2008, 'Podocytes use FcRn to clear IgG from the glomerular basement membrane', P NATL ACAD SCI USA, Jg. 105, Nr. 3, S. 967-72. https://doi.org/10.1073/pnas.0711515105

APA

Akilesh, S., Huber, T. B., Wu, H., Wang, G., Hartleben, B., Kopp, J. B., Miner, J. H., Roopenian, D. C., Unanue, E. R., & Shaw, A. S. (2008). Podocytes use FcRn to clear IgG from the glomerular basement membrane. P NATL ACAD SCI USA, 105(3), 967-72. https://doi.org/10.1073/pnas.0711515105

Vancouver

Akilesh S, Huber TB, Wu H, Wang G, Hartleben B, Kopp JB et al. Podocytes use FcRn to clear IgG from the glomerular basement membrane. P NATL ACAD SCI USA. 2008 Jan 22;105(3):967-72. https://doi.org/10.1073/pnas.0711515105

Bibtex

@article{22cd9c2659434ecaab736d959e5b5e95,
title = "Podocytes use FcRn to clear IgG from the glomerular basement membrane",
abstract = "The glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM). Here, we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged, and tracer studies showed delayed clearance of IgG from the kidneys of FcRn-deficient mice. Supporting a role for this pathway in disease, saturating the clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery is likely to be a common mechanism promoting glomerular diseases.",
keywords = "Animals, Cell Line, Female, Glomerular Basement Membrane, Histocompatibility Antigens Class I, Immunoglobulin G, Mice, Mice, Knockout, Nephritis, Podocytes, Protein Transport, Receptors, Fc, Sensitivity and Specificity, Serum, Journal Article, Research Support, N.I.H., Extramural",
author = "Shreeram Akilesh and Huber, {Tobias B} and Hui Wu and Gary Wang and Bj{\"o}rn Hartleben and Kopp, {Jeffrey B} and Miner, {Jeffrey H} and Roopenian, {Derry C} and Unanue, {Emil R} and Shaw, {Andrey S}",
year = "2008",
month = jan,
day = "22",
doi = "10.1073/pnas.0711515105",
language = "English",
volume = "105",
pages = "967--72",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "3",

}

RIS

TY - JOUR

T1 - Podocytes use FcRn to clear IgG from the glomerular basement membrane

AU - Akilesh, Shreeram

AU - Huber, Tobias B

AU - Wu, Hui

AU - Wang, Gary

AU - Hartleben, Björn

AU - Kopp, Jeffrey B

AU - Miner, Jeffrey H

AU - Roopenian, Derry C

AU - Unanue, Emil R

AU - Shaw, Andrey S

PY - 2008/1/22

Y1 - 2008/1/22

N2 - The glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM). Here, we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged, and tracer studies showed delayed clearance of IgG from the kidneys of FcRn-deficient mice. Supporting a role for this pathway in disease, saturating the clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery is likely to be a common mechanism promoting glomerular diseases.

AB - The glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM). Here, we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged, and tracer studies showed delayed clearance of IgG from the kidneys of FcRn-deficient mice. Supporting a role for this pathway in disease, saturating the clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery is likely to be a common mechanism promoting glomerular diseases.

KW - Animals

KW - Cell Line

KW - Female

KW - Glomerular Basement Membrane

KW - Histocompatibility Antigens Class I

KW - Immunoglobulin G

KW - Mice

KW - Mice, Knockout

KW - Nephritis

KW - Podocytes

KW - Protein Transport

KW - Receptors, Fc

KW - Sensitivity and Specificity

KW - Serum

KW - Journal Article

KW - Research Support, N.I.H., Extramural

U2 - 10.1073/pnas.0711515105

DO - 10.1073/pnas.0711515105

M3 - SCORING: Journal article

C2 - 18198272

VL - 105

SP - 967

EP - 972

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 3

ER -