A critical role for complement in maintenance of self-tolerance

Andrey P. Prodeus; Siegfried Goerg; Li Ming Shen; Olga O. Pozdnyakova; Lisa Chu; Elisabeth M. Alicot; Christopher C. Goodnow; Michael C. Carroll

doi:10.1016/S1074-7613(00)80669-X

A critical role for complement in maintenance of self-tolerance

Andrey P. Prodeus, Siegfried Goerg, Li Ming Shen, Olga O. Pozdnyakova, Lisa Chu, Elisabeth M. Alicot, Christopher C. Goodnow, Michael C. Carroll^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

330 Citations (Scopus)

Abstract

The role of complement in the maintenance of self-tolerance has been examined in two models: an immunoglobulin transgenic model of peripheral tolerance and a lupus-like murine model of CD95 (Fas) deficiency. We find that self-reactive B lymphocytes deficient in complement receptors CD21/CD35 or transferred into mice deficient in the complement protein C4 are not anergized by soluble self-antigen. In the second model, deficiency in CD21/CD35 or C4 combined with CD95 deficiency results in high titers of anti- nuclear antibodies leading to severe lupus-like disease. These findings suggest a novel role for the complement system in B cell tolerance and provide insight into the genetic association of complement deficiency with susceptibility to systemic lupus erythematosus.

Original language	English
Pages (from-to)	721-731
Number of pages	11
Journal	Immunity
Volume	9
Issue number	5
DOIs	https://doi.org/10.1016/S1074-7613(00)80669-X
Publication status	Published - Nov 1998

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title = "A critical role for complement in maintenance of self-tolerance",

abstract = "The role of complement in the maintenance of self-tolerance has been examined in two models: an immunoglobulin transgenic model of peripheral tolerance and a lupus-like murine model of CD95 (Fas) deficiency. We find that self-reactive B lymphocytes deficient in complement receptors CD21/CD35 or transferred into mice deficient in the complement protein C4 are not anergized by soluble self-antigen. In the second model, deficiency in CD21/CD35 or C4 combined with CD95 deficiency results in high titers of anti- nuclear antibodies leading to severe lupus-like disease. These findings suggest a novel role for the complement system in B cell tolerance and provide insight into the genetic association of complement deficiency with susceptibility to systemic lupus erythematosus.",

author = "Prodeus, {Andrey P.} and Siegfried Goerg and Shen, {Li Ming} and Pozdnyakova, {Olga O.} and Lisa Chu and Alicot, {Elisabeth M.} and Goodnow, {Christopher C.} and Carroll, {Michael C.}",

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T1 - A critical role for complement in maintenance of self-tolerance

AU - Prodeus, Andrey P.

AU - Goerg, Siegfried

AU - Shen, Li Ming

AU - Pozdnyakova, Olga O.

AU - Chu, Lisa

AU - Alicot, Elisabeth M.

AU - Goodnow, Christopher C.

AU - Carroll, Michael C.

PY - 1998/11

Y1 - 1998/11

N2 - The role of complement in the maintenance of self-tolerance has been examined in two models: an immunoglobulin transgenic model of peripheral tolerance and a lupus-like murine model of CD95 (Fas) deficiency. We find that self-reactive B lymphocytes deficient in complement receptors CD21/CD35 or transferred into mice deficient in the complement protein C4 are not anergized by soluble self-antigen. In the second model, deficiency in CD21/CD35 or C4 combined with CD95 deficiency results in high titers of anti- nuclear antibodies leading to severe lupus-like disease. These findings suggest a novel role for the complement system in B cell tolerance and provide insight into the genetic association of complement deficiency with susceptibility to systemic lupus erythematosus.

AB - The role of complement in the maintenance of self-tolerance has been examined in two models: an immunoglobulin transgenic model of peripheral tolerance and a lupus-like murine model of CD95 (Fas) deficiency. We find that self-reactive B lymphocytes deficient in complement receptors CD21/CD35 or transferred into mice deficient in the complement protein C4 are not anergized by soluble self-antigen. In the second model, deficiency in CD21/CD35 or C4 combined with CD95 deficiency results in high titers of anti- nuclear antibodies leading to severe lupus-like disease. These findings suggest a novel role for the complement system in B cell tolerance and provide insight into the genetic association of complement deficiency with susceptibility to systemic lupus erythematosus.

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DO - 10.1016/S1074-7613(00)80669-X

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VL - 9

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JO - Immunity

JF - Immunity

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A critical role for complement in maintenance of self-tolerance

Abstract

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