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The Journal of Immunology, 2002, 169: 3492-3498.
Copyright © 2002 by The American Association of Immunologists

Optimal Colocalization of TCR and CD8 as a Novel Mechanism for the Control of Functional Avidity1

Andrew G. Cawthon and Martha A. Alexander-Miller2

Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157

The improved efficacy of high avidity CTL for clearance of virus has been well-documented. Thus, elucidation of the mechanisms that confer the increased sensitivity to peptide ligand demonstrated by high avidity CTL is critical. Using CTL lines of high and low avidity generated from a TCR transgenic mouse, we have found that functional avidity can be controlled by the expression of CD8{alpha}{alpha} vs CD8{alpha}{beta} and the ability of CTLs to colocalize the TCR and CD8 in the membrane. Colocalization of these molecules was mediated by lipid rafts and importantly, raft disruption resulted in the conversion of high avidity CTL into a lower functional avidity phenotype. These novel findings provide insights into the control of functional avidity in response to viral infection.




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