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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 Huber,  
 

CD1d expression on hemopoietic cells promotes CD4+ Th1 response in coxsackievirus B3 induced myocarditis.

Coxsackievirus B3 induced murine myocarditis depends upon CD1d expression and upon a population of CD1d-restricted Vgamma4+ T cells. Infection upregulates CD1d expression in CD4+ T cells. Bone marrow chimeras were made between BALB/c and BALB/c CD1d-/- mice and showed that CD1d expression in either hemopoietic and non-hemopoietic cells induces myocarditis, although CD1d expression on hemopoietic cells was more effective in increasing Vgamma4+ cell numbers and activation, and CD4+ IFNgamma+ cell response than CD1d expression on non-hemopoietic cells. Co-culture of enriched CD4+ cells from infected CD1d-/- and BALB/c mice with Vgamma4+ T cells demonstrated that the Vgamma4+ cells bias the CD4+ cell response to the Th1 phenotype through CD1d. Anti-CD1d antibody effectively blocked promotion of IFNgamma expression by the CD4+ cell population. These results show that Vgamma4+ cells modulate developing adaptive immunity through recognition of CD1d on CD4+ T cells, and that this interaction, more than Vgamma4+ cell interaction with infected cardiocytes, determines pathogenicity.[1]

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