ICOS co-stimulatory receptor is essential for T-cell activation and function

Chen Dong, Amy E. Juedes, Ulla-Angela Temann, Sujan Shresta, James P. Allison, Nancy H. Ruddle and Richard A. Flavell ()
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Chen Dong: Howard Hughes Medical Institute, Section of Immunobiology
Amy E. Juedes: Yale University School of Medicine
Ulla-Angela Temann: Howard Hughes Medical Institute, Section of Immunobiology
Sujan Shresta: University of California at Berkeley
James P. Allison: University of California at Berkeley
Nancy H. Ruddle: Yale University School of Medicine
Richard A. Flavell: Howard Hughes Medical Institute, Section of Immunobiology

Nature, 2001, vol. 409, issue 6816, 97-101

Abstract: Abstract T-lymphocyte activation and immune function are regulated by co-stimulatory molecules. CD28, a receptor for B7 gene products, has a chief role in initiating T-cell immune responses1,2. CTLA4, which binds B7 with a higher affinity, is induced after T-cell activation and is involved in downregulating T-cell responses3,4. The inducible co-stimulatory molecule (ICOS), a third member of the CD28/CTLA4 family, is expressed on activated T cells5,6. Its ligand B7H/B7RP-1 is expressed on B cells and in non-immune tissues after injection of lipopolysaccharide into animals6,7. To understand the role of ICOS in T-cell activation and function, we generated and analysed ICOS-deficient mice. Here we show that T-cell activation and proliferation are defective in the absence of ICOS. In addition, ICOS-/- T cells fail to produce interleukin-4 when differentiated in vitro or when primed in vivo. ICOS is required for humoral immune responses after immunization with several antigens. ICOS-/- mice showed greatly enhanced susceptibility to experimental autoimmune encephalomyelitis, indicating that ICOS has a protective role in inflammatory autoimmune diseases.

Date: 2001
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DOI: 10.1038/35051100

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