# TUMOR-SPECIFIC CTL RECOGNITION OF TRANSFECTED CELLS

> **NIH NIH R01** · DANA-FARBER CANCER INST · 1988 · $133,437

## Abstract

Cytotoxic T lymphocytes (CTL or killer T lymphocytes) play a critical role
in the rejection of virally-induced tumors and the elimination of viral
infections by the host.  Yet the way in which CTL recognize their targets
is unknown.  Indeed, even which viral or tumor viral protein (if any) is
recognized by CTL is not clear.  Part of the difficulty involved in the
study of CTL interaction with virus-infected cells or tumors lies in the
number of viral proteins made by the virus, our inability to modulate the
expression of these proteins, and the cytopathic effects induced by these
viruses.  These problems have been overcome by a system we have developed
that utilizes cloned viral genes to allow expression of single viral
proteins on the surface of uninfected (and nontumor) mouse cells.
Preliminary data shows that such cells are recognized and killed by
virus-specific or tumor-specific CTL, as if they were true infected cells
or tumor cells.  It is possible to alter the levels of antigen expression
in these cells.  The system also facilitates the use of in vitro,
site-directed mutagenesis to alter the viral gene products.  This technique
provides a new and powerful way of studying cell-mediated host defenses
against viral infections and tumors.  This model system is being used to
probe CTL-target cell interactions and will establish:  (1) which virus or
tumor virus proteins are being recognized by CTL; (2) the number of antigen
molecules per cell required for CTL recognition; (3) the presence or
absence of physical association between the viral antigens and the cellular
H-2 antigens and the hierarchy of such associations; and (4) which
structural areas on the viral antigen are being recognized by CTL and
whether they differ from the areas recognized by antibodies.  Establishing
the answers to such basic questions is vital if we are to understand the
way in which CTL carry out their immune surveillance against infections and
tumors, why some tumors and not others are destroyed, and the possible ways
in which CTL-mediated destruction of infected cells or tumors could be
augmented in the patient.  Our ability to selectively mutagenize the viral
genes and present them more physiologically to CTL precursors (i.e., on a
cell membrane and in the context of H-2 antigens) could be used to possibly
enhance the host response to malignancy and lead to the development of a
T-cell-specific vaccine.  (AG)

## Key facts

- **NIH application ID:** 3174950
- **Project number:** 3R01CA037169-04S1
- **Recipient organization:** DANA-FARBER CANCER INST
- **SAM.gov UEI:** DPMGH9MG1X67
- **Principal Investigator:** Douglas V Faller
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $133,437
- **Award type:** 3
- **Project period:** 1984-04-01 → 1989-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3174950

## Citation

> US National Institutes of Health, RePORTER application 3174950, TUMOR-SPECIFIC CTL RECOGNITION OF TRANSFECTED CELLS (3R01CA037169-04S1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3174950. Licensed CC0.

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