129/SvJ mice have mutated CD23 and hyper IgE

Jill W. Ford; Jamie L. Sturgill; Daniel H. Conrad

doi:10.1016/j.cellimm.2008.08.003

129/SvJ mice have mutated CD23 and hyper IgE

Jill W. Ford
, Jamie L. Sturgill
, Daniel H. Conrad

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

19 Scopus citations

Abstract

CD23, the low affinity IgE receptor, is hypothesized to function as a negative regulator of IgE production. Upon discovering reduced CD23 surface levels in 129/SvJ inbred mice, we sought to further investigate 129/SvJ CD23 and to examine its influence on IgE levels. Five amino acid substitutions were found in 129/SvJ CD23. Identical mutations were also observed in CD23 from New Zealand Black and 129P1/ReJ mice. 129/SvJ B cells proliferated more rapidly than those from BALB/c after stimulation with IL-4 and CD40 ligand trimer. However, in vitro IgE levels in supernatants from stimulated 129/SvJ B cells were significantly reduced. Contrary to the in vitro findings, the 129/SvJ CD23 mutations correlated with a hyper IgE phenotype in vivo and 129/SvJ were able to clear Nippostrongylus brasiliensis infection more rapidly than either BALB/c or C57BL/6. Overall, this study further suggests that CD23 is an important regulatory factor for IgE production.

Original language	English
Pages (from-to)	124-134
Number of pages	11
Journal	Cellular Immunology
Volume	254
Issue number	2
DOIs	https://doi.org/10.1016/j.cellimm.2008.08.003
State	Published - 2009

Bibliographical note

Funding Information:
We thank Jerome Schlomer, Witemba Kabange, Yvette Orihuela, Dae-Jong Kang, and Joel Mathews for excellent technical assistance. This work was supported by the U.S. Public Health Service Grant AI18697. J.W.F. was supported in part by the National Institute of Allergy and Infectious Diseases Training Grant T32AI007407.

Funding

We thank Jerome Schlomer, Witemba Kabange, Yvette Orihuela, Dae-Jong Kang, and Joel Mathews for excellent technical assistance. This work was supported by the U.S. Public Health Service Grant AI18697. J.W.F. was supported in part by the National Institute of Allergy and Infectious Diseases Training Grant T32AI007407.

Funders	Funder number
Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases	T32AI007407
Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases
U.S. Public Health Service	AI18697
U.S. Public Health Service

Keywords

129/SvJ mouse
B cells
CD23
Helminth
Hyper IgE

ASJC Scopus subject areas

Immunology

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10.1016/j.cellimm.2008.08.003

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title = "129/SvJ mice have mutated CD23 and hyper IgE",

abstract = "CD23, the low affinity IgE receptor, is hypothesized to function as a negative regulator of IgE production. Upon discovering reduced CD23 surface levels in 129/SvJ inbred mice, we sought to further investigate 129/SvJ CD23 and to examine its influence on IgE levels. Five amino acid substitutions were found in 129/SvJ CD23. Identical mutations were also observed in CD23 from New Zealand Black and 129P1/ReJ mice. 129/SvJ B cells proliferated more rapidly than those from BALB/c after stimulation with IL-4 and CD40 ligand trimer. However, in vitro IgE levels in supernatants from stimulated 129/SvJ B cells were significantly reduced. Contrary to the in vitro findings, the 129/SvJ CD23 mutations correlated with a hyper IgE phenotype in vivo and 129/SvJ were able to clear Nippostrongylus brasiliensis infection more rapidly than either BALB/c or C57BL/6. Overall, this study further suggests that CD23 is an important regulatory factor for IgE production.",

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note = "Funding Information: We thank Jerome Schlomer, Witemba Kabange, Yvette Orihuela, Dae-Jong Kang, and Joel Mathews for excellent technical assistance. This work was supported by the U.S. Public Health Service Grant AI18697. J.W.F. was supported in part by the National Institute of Allergy and Infectious Diseases Training Grant T32AI007407.",

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AU - Sturgill, Jamie L.

AU - Conrad, Daniel H.

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PY - 2009

Y1 - 2009

N2 - CD23, the low affinity IgE receptor, is hypothesized to function as a negative regulator of IgE production. Upon discovering reduced CD23 surface levels in 129/SvJ inbred mice, we sought to further investigate 129/SvJ CD23 and to examine its influence on IgE levels. Five amino acid substitutions were found in 129/SvJ CD23. Identical mutations were also observed in CD23 from New Zealand Black and 129P1/ReJ mice. 129/SvJ B cells proliferated more rapidly than those from BALB/c after stimulation with IL-4 and CD40 ligand trimer. However, in vitro IgE levels in supernatants from stimulated 129/SvJ B cells were significantly reduced. Contrary to the in vitro findings, the 129/SvJ CD23 mutations correlated with a hyper IgE phenotype in vivo and 129/SvJ were able to clear Nippostrongylus brasiliensis infection more rapidly than either BALB/c or C57BL/6. Overall, this study further suggests that CD23 is an important regulatory factor for IgE production.

AB - CD23, the low affinity IgE receptor, is hypothesized to function as a negative regulator of IgE production. Upon discovering reduced CD23 surface levels in 129/SvJ inbred mice, we sought to further investigate 129/SvJ CD23 and to examine its influence on IgE levels. Five amino acid substitutions were found in 129/SvJ CD23. Identical mutations were also observed in CD23 from New Zealand Black and 129P1/ReJ mice. 129/SvJ B cells proliferated more rapidly than those from BALB/c after stimulation with IL-4 and CD40 ligand trimer. However, in vitro IgE levels in supernatants from stimulated 129/SvJ B cells were significantly reduced. Contrary to the in vitro findings, the 129/SvJ CD23 mutations correlated with a hyper IgE phenotype in vivo and 129/SvJ were able to clear Nippostrongylus brasiliensis infection more rapidly than either BALB/c or C57BL/6. Overall, this study further suggests that CD23 is an important regulatory factor for IgE production.

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KW - CD23

KW - Helminth

KW - Hyper IgE

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129/SvJ mice have mutated CD23 and hyper IgE

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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