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The Journal of Immunology, 2004, 173: 5923-5928.
Copyright © 2004 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Tumor-Specific CTL Are Constitutively Cross-Armed in Draining Lymph Nodes and Transiently Disseminate to Mediate Tumor Regression following Systemic CD40 Activation1

Philip A. Stumbles2,*, Robyn Himbeck*,{dagger}, Jeffrey A. Frelinger{ddagger}, Edward J. Collins{ddagger}, Richard A. Lake*,{dagger} and Bruce W. S. Robinson2,*,{dagger}

* School of Medicine and Pharmacology, University of Western Australia, Sir Charles Gairdner Hospital, and {dagger} Western Australian Institute for Medical Research, Sir Charles Gairdner Hospital, Perth, Western Australia; and {ddagger} Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599

The cross-arming of effector CTL in response to cross-presented tumor Ags is predicted to fail in the absence of CD40 stimulation. However, questions remain regarding the role of CD40 signaling and additional CD4+ T cell-derived signals in this process. To address this, we have analyzed the cross-arming of tumor-specific CTL effectors in vivo in a mouse model of established tumor and tumor regression following CD40 activation. We found that tumor-specific CTL were constitutively cross-armed in tumor-draining lymph nodes during tumor growth and that systemic CD40 activation did not alter CTL cross-arming in the tumor-draining lymph nodes. Rather, CD40 activation induced peripheral dissemination of tumor-specific CTL effectors that required continual CD40 stimulation to maintain peripheral CTL and tumor regression. These data indicate that CD40 activation enhances the peripheral survival of constitutively cross-armed CTL and that persistent CD4+ T cell signals are required for their long-term activity.




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