# THE CELLULAR BASIS OF DELAYED-TYPE HYPERSENSITIVITY

> **NIH NIH R01** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 1987 · $244,209

## Abstract

Previous work on this grant indicated that natural killer (NK) cells are
heterogeneous and have a potentially important role to play in mediating
rejection of virus infected cells and restricting metastases of tumor
cells.  The overall aim of this application is to provide insight into the
nature and capability of various NK cell subsets; the means by which they
discriminate between virus infected an uninfected cells, and between
neoplastic and nonneoplastic cells; the mechanisms of regulation of NK
activity of these sets; and ultimately their functional role of resistance
to virus infection and tumor cells in vivo.  Where appropriate we will
attempt to develop continuous murine and human NK cell lines of vrious NK
phenotypes, study their regulation by IFN and IL-2, and attempt to
delineate which subsets produce interferon and the pathways of
differentiation as determined by cell surface markers.  For studies of the
nature of target cell recognition we will use target cells infected by a
variety of viruses and viral mutants, and target cells transformed with
fragments of oncogenic viral DNA to establish the relationship between
events in neoplastic transformation and recognition by NK cells.  For
studies of the role of NK cells in vivo, we will examine primary mouse and
human tumors and metastases from the same individual for susceptibility to
NK cells in both beige mice and nude mice immunosuppressed for NK activity
and will characterize mechanism of resistance to the growth tumors and
metastases by adoptive transfers with defined lymphocyte subpopulations.
Possible defects in the functioning of the IFN-NK system in patients with
putative persistent viral diseases, multiple sclerosis and systemic lupus
erythematosus will be pursued.

## Key facts

- **NIH application ID:** 3124618
- **Project number:** 5R01AI009807-18
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** BARRY R. BLOOM
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $244,209
- **Award type:** 5
- **Project period:** 1983-06-01 → 1988-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124618

## Citation

> US National Institutes of Health, RePORTER application 3124618, THE CELLULAR BASIS OF DELAYED-TYPE HYPERSENSITIVITY (5R01AI009807-18). Retrieved via MORVS 2026-10-26 from https://api.morvs.ai/grant/nih/3124618. Licensed CC0.

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