# GAMMA INTERFERON RECEPTOR ON TUMORILYTIC MACROPHAGES

> **NIH NIH R01** · UNIVERSITY OF KANSAS MEDICAL CENTER · 1990 · $170,680

## Abstract

The long range goal of the proposed research is to learn how the gamma
interferon receptor is involved in the regulation of macrophage activation
for tumor cell killing.  The rationale for undertaking the proposed
research is that murine gamma interferon (MuIFN-gamma), which is one form
of macrophage activating factor, mediates its effects through a membrane
receptor.  Investigation of the receptor should, therefore, yield
information that is pertinent to identifying the early events that are
involved in the induction of macrophage activation.  The availability of
large amounts of recombinant murine gamma interferon from Genentech Inc.,
as well as homogenous populations of cultured macrophages have made these
studies feasible.  They will include:  (1) receptor binding studies,
designed to quantify the number and binding affinity of MuIFN-gamma
receptors on unstimulated macrophages, as well as those with either
increased responsiveness to MuIFN-gamma (inflammatory macrophages) or
diminished responsiveness (postcytolytlc macrophages).  Computer-assisted
analysis (LIGAND program) of Scatchard plots will be the principal approach
here; (2) enrichment of the MuIFN-gamma receptor complex from macrophage
membranes, either with or without chemical crosslinking; (3) preparation of
monoclonal antibodies against the receptor. These monoclonal antibodies
will be used to immunopurify the receptor, as well as to determine whether
or not antireceptor antibody binding can functionally mimic binding of
MuIFN-gamma; and (4) partial physicochemical and biochemical
characterization of the isolated MuIFN-gamma receptor.  If time allows,
additional studies will be performed to preliminarily characterize the
receptor with regard to its functional type.  With general indications as
to the functional type, it should then be possible to design definitive
studies that will show how the receptor initiates the events that induce
activation.  The proposed research is significant because it will yield
new, basic information about an important host defense mechanism,
macrophage activation for tumor cell killing.  It is expected that much of
the knowledge obtained will be equally applicable to understanding how
MuIFN-gamma modulates a variety of other macrophage characteristics and
functions, ranging from induction of an antiviral state to phagocytes or
antigen presentation.  To our knowledge, these will be the first studies of
the gamma interferon receptor on macrophages.  (HF)

## Key facts

- **NIH application ID:** 3177051
- **Project number:** 5R01CA038779-05
- **Recipient organization:** UNIVERSITY OF KANSAS MEDICAL CENTER
- **SAM.gov UEI:** YXJGGNC5J269
- **Principal Investigator:** STEPHEN W RUSSELL
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $170,680
- **Award type:** 5
- **Project period:** 1988-02-01 → 1991-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3177051

## Citation

> US National Institutes of Health, RePORTER application 3177051, GAMMA INTERFERON RECEPTOR ON TUMORILYTIC MACROPHAGES (5R01CA038779-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3177051. Licensed CC0.

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