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The Journal of Immunology, 2002, 168: 1557-1565.
Copyright © 2002 by The American Association of Immunologists

Differential SLP-76 Expression and TCR-Mediated Signaling in Effector and Memory CD4 T Cells1

S. Farzana Hussain*, Charles F. Anderson{dagger} and Donna L. Farber2,*

* Department of Surgery, University of Maryland, Baltimore, MD 21201; and {dagger} Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742

We present in this study novel findings on TCR-mediated signaling in naive, effector, and memory CD4 T cells that identify critical biochemical markers to distinguish these subsets. We demonstrate that relative to naive CD4 T cells, memory CD4 T cells exhibit a profound decrease in expression of the linker/adapter molecule SLP-76, while effector T cells express normal to elevated levels of SLP-76. The reduced level of SLP-76 is memory CD4 T cells is coincident with reduced phosphorylation overall, yet the residual SLP-76 couples to a subset of TCR-associated linker molecules, leading to downstream mitogen-activated protein (MAP) kinase activation. By contrast, effector CD4 T cells strongly phosphorylate SLP-76, linker for activation of T cells, and additional Grb2-coupled proteins, exhibit increased associations of SLP-76 to phosphorylated linkers, and hyperphosphorylate downstream Erk1/2 MAP kinases. Our results suggest distinct coupling of signaling intermediates to the TCR in naive, effector, and memory CD4 T cells. Whereas effector CD4 T cells amplify existing TCR signaling events accounting for rapid effector responses, memory T cells engage fewer signaling intermediates to efficiently link TCR triggering directly to downstream MAP kinase activation.




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