ICOS is critical for CD40-mediated antibody class switching View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-01

AUTHORS

Alexander J. McAdam, Rebecca J. Greenwald, Michele A. Levin, Tatyana Chernova, Nelly Malenkovich, Vincent Ling, Gordon J. Freeman, Arlene H. Sharpe

ABSTRACT

The inducible co-stimulatory molecule (ICOS) is a CD28 homologue implicated in regulating T-cell differentiation. Because co-stimulatory signals are critical for regulating T-cell activation, an understanding of co-stimulatory signals may enable the design of rational therapies for immune-mediated diseases. According to the two-signal model for T-cell activation, T cells require an antigen-specific signal and a second, co-stimulatory, signal for optimal T-cell activation. The co-stimulatory signal promotes T-cell proliferation, lymphokine secretion and effector function. The B7-CD28 pathway provides essential signals for T-cell activation, but does not account for all co-stimulation. We have generated mice lacking ICOS (ICOS-/- ) to determine the essential functions of ICOS. Here we report that ICOS-/- mice exhibit profound deficits in immunoglobulin isotype class switching, accompanied by impaired germinal centre formation. Class switching was restored in ICOS-/- mice by CD40 stimulation, showing that ICOS promotes T-cell/B-cell collaboration through the CD40/CD40L pathway. More... »

PAGES

102

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/35051107

DOI

http://dx.doi.org/10.1038/35051107

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009086703

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11343122


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