TY - JOUR
T1 - Regulation of immune and autoimmune responses by ICOS
AU - Dong, Chen
AU - Nurieva, Roza I.
N1 - Funding Information:
We thank our many collaborators for scientific contribution, Caroline Bishop for critical reading of the manuscript, and the entire Dong Lab for discussion and help. Our work is supported in part by grants from National Institute of Health. C. Dong is a recipient of an Arthritis Investigator award from Arthritis Foundation.
PY - 2003/11
Y1 - 2003/11
N2 - Proper T cell activation and function are regulated by the innate immune system, importantly through positive and negative costimulatory molecules in the B7 superfamily. Inducible costimulator (ICOS), the receptor for B7h (also known as B7RP-1), is expressed on T cells after T cell activation. Recently, using ICOS-deficient mice, we have examined the roles of ICOS in immune responses. ICOS is required for humoral immunity. In organ-specific autoimmune responses, however, ICOS has contrast roles in different disease models. On the one hand, ICOS-/- mice exhibited extreme sensitivity to experimental autoimmune encephalomyelitis (EAE); on the other, ICOS gene deletion led to complete resistance to collagen-induced arthritis (CIA) in mice. Our work not only illustrates the complexity of immune regulation by costimulatory molecules, but also suggests novel therapeutic strategies for various autoimmune diseases.
AB - Proper T cell activation and function are regulated by the innate immune system, importantly through positive and negative costimulatory molecules in the B7 superfamily. Inducible costimulator (ICOS), the receptor for B7h (also known as B7RP-1), is expressed on T cells after T cell activation. Recently, using ICOS-deficient mice, we have examined the roles of ICOS in immune responses. ICOS is required for humoral immunity. In organ-specific autoimmune responses, however, ICOS has contrast roles in different disease models. On the one hand, ICOS-/- mice exhibited extreme sensitivity to experimental autoimmune encephalomyelitis (EAE); on the other, ICOS gene deletion led to complete resistance to collagen-induced arthritis (CIA) in mice. Our work not only illustrates the complexity of immune regulation by costimulatory molecules, but also suggests novel therapeutic strategies for various autoimmune diseases.
KW - Collagen-induced arthritis
KW - Costimulation
KW - Experimental autoimmune encephalomyelitis
KW - IL-17
KW - T cells
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U2 - 10.1016/S0896-8411(03)00119-7
DO - 10.1016/S0896-8411(03)00119-7
M3 - Article
C2 - 14599850
AN - SCOPUS:0242486678
SN - 0896-8411
VL - 21
SP - 255
EP - 260
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
IS - 3
ER -