Abstract

CD28/B7 costimulation has been implicated in the induction and progression of autoimmune diseases. Experimentally induced models of autoimmunity have been shown to be prevented or reduced in intensity in mice rendered deficient for CD28 costimulation. In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. These cells are absent from both CD28KO and B7-1/B7-2KO mice, and the transfer of this regulatory T cell subset from control NOD animals into CD28-deficient animals can delay/prevent diabetes. The results suggest that the CD28/ B7 costimulatory pathway is essential for the development and homeostasis of regulatory T cells that control spontaneous autoimmune diseases.

Keywords

CD28NodNOD miceAutoimmunityIL-2 receptorImmunologyBiologyHomeostasisDiabetes mellitusType 1 diabetesT cellCell biologyImmune systemEndocrinology

MeSH Terms

AbataceptAnimalsAntigensCDAntigensDifferentiationAutoimmune DiseasesB7-1 AntigenB7-2 AntigenCD28 AntigensCD4-Positive T-LymphocytesCTLA-4 AntigenDiabetes MellitusType 1FemaleHomeostasisImmunoconjugatesLymphocyte ActivationLymphokinesMaleMembrane GlycoproteinsMiceMiceInbred NODMiceKnockoutPrediabetic StateReceptorsInterleukin-2

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Publication Info

Year
2000
Type
article
Volume
12
Issue
4
Pages
431-440
Citations
2028
Access
Closed

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2028
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102
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1628
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Cite This

Benoı̂t L. Salomon, Deborah J. Lenschow, Lesley Rhee et al. (2000). B7/CD28 Costimulation Is Essential for the Homeostasis of the CD4+CD25+ Immunoregulatory T Cells that Control Autoimmune Diabetes. Immunity , 12 (4) , 431-440. https://doi.org/10.1016/s1074-7613(00)80195-8

Identifiers

DOI
10.1016/s1074-7613(00)80195-8
PMID
10795741

Data Quality

Data completeness: 86%