Contribution of the innate immune system to autoimmune diabetes: A role for the CR1/CR2 complement receptors

Hooman Noorchashm; Daniel J. Moore; Yen K. Lieu; Negin Noorchashm; Alexander Schlachterman; Howard K. Song; John D. Lambris; Clyde F. Barker; Ali Naji

doi:10.1006/cimm.1999.1522

Contribution of the innate immune system to autoimmune diabetes: A role for the CR1/CR2 complement receptors

Hooman Noorchashm
, Daniel J. Moore
, Yen K. Lieu
, Negin Noorchashm
, Alexander Schlachterman
, Howard K. Song
, John D. Lambris
, Clyde F. Barker
, Ali Naji

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

37 Scopus citations

Abstract

B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell- mediated attack on islet β cells of NOD mice.

Original language	English (US)
Pages (from-to)	75-79
Number of pages	5
Journal	Cellular Immunology
Volume	195
Issue number	1
DOIs	https://doi.org/10.1006/cimm.1999.1522
State	Published - Jul 10 1999
Externally published	Yes

Funding

1 This work was supported by Grants DK34878 and DK54215 from the National Institutes of Health and Juvenile Diabetes Foundation International. H.N. was supported by Training Grant NEI T32 from the National Eye Institute. 2 Abbreviations used: NOD, nonobese diabetic; MFI, mean floures-cence index.

Funders	Funder number
National Institutes of Health and Juvenile Diabetes Foundation International	NEI T32
National Eye Institute and Casey Eye Institute

ASJC Scopus subject areas

Immunology

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10.1006/cimm.1999.1522

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@article{b8fff4807bb442f8a58318db66295484,

title = "Contribution of the innate immune system to autoimmune diabetes: A role for the CR1/CR2 complement receptors",

abstract = "B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell- mediated attack on islet β cells of NOD mice.",

author = "Hooman Noorchashm and Moore, \{Daniel J.\} and Lieu, \{Yen K.\} and Negin Noorchashm and Alexander Schlachterman and Song, \{Howard K.\} and Lambris, \{John D.\} and Barker, \{Clyde F.\} and Ali Naji",

note = "Funding Information: 1 This work was supported by Grants DK34878 and DK54215 from the National Institutes of Health and Juvenile Diabetes Foundation International. H.N. was supported by Training Grant NEI T32 from the National Eye Institute. 2 Abbreviations used: NOD, nonobese diabetic; MFI, mean floures-cence index.",

year = "1999",

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doi = "10.1006/cimm.1999.1522",

language = "English (US)",

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T2 - A role for the CR1/CR2 complement receptors

AU - Noorchashm, Hooman

AU - Moore, Daniel J.

AU - Lieu, Yen K.

AU - Noorchashm, Negin

AU - Schlachterman, Alexander

AU - Song, Howard K.

AU - Lambris, John D.

AU - Barker, Clyde F.

AU - Naji, Ali

N1 - Funding Information: 1 This work was supported by Grants DK34878 and DK54215 from the National Institutes of Health and Juvenile Diabetes Foundation International. H.N. was supported by Training Grant NEI T32 from the National Eye Institute. 2 Abbreviations used: NOD, nonobese diabetic; MFI, mean floures-cence index.

PY - 1999/7/10

Y1 - 1999/7/10

N2 - B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell- mediated attack on islet β cells of NOD mice.

AB - B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell- mediated attack on islet β cells of NOD mice.

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JO - Cellular Immunology

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Contribution of the innate immune system to autoimmune diabetes: A role for the CR1/CR2 complement receptors

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