Published online before print August 4, 2005
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Department of Microbiology, University of Tennessee, Knoxville
1Correspondence: M409 Department of Microbiology, University of Tennessee, Knoxville, TN 37996; Department of Microbiology, James Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614. E-mail: udayk@utk.edu and btr{at}utk.edu
The magnitude and efficacy of CD8+ T cell memory may notably regress, especially if immune induction occurs in the absence of adequate CD4+ help. This report demonstrates that this CD8+ memory malfunction could be remedied if a source of cognate antigen-recognizing helper cells were provided during recall. The inability of adoptive transfer of memory SIINFEKL-specific CD8 cells to reject tumors was overcome if recipients were primed for ovalbumin-specific helper cell responses. Additionally, animals primed for a SIINFEKL-specific memory response and incapable of rejecting the tumor could regain protective immunity if given helper cells. This pattern of CD8+ T cell functional rescue or reprogramming by helper cell transfer was replicated using a Herpes simplex virus antiviral immunity system. Our results could mean that therapeutic vaccine approaches could be designed to compensate situations that have defective CD8+ T cell function.
Key Words: vaccine HSV
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