EFFECTOR AND SUPPRESSOR MECHANISM IN TUMOR IMMUNITY

NIH RePORTER · NIH · R01 · $85,723 · view on reporter.nih.gov ↗

Abstract

Our studies on tumor immunity in vitro and in vivo led to the observation that macrophages were generated in vivo in tumor bearing mice and in vitro in spleen cell cultures. The macrophages are generated in several stages involving radiosensitive and radio- resistant maturation. They can be activated to inhibit tumor cell growth in a local or contact dependent manner and can be activated to produce monokines required for cellular immune responses. T cells can activate the macrophages by direct recognition of allo- MHC determinants or by recognition of antigen in association with self determinants. Using T cell clones, flow cytometric sorting of cells from primary lymphoid tissue, and in vitro culture techniques, functionally distinct and maturationally distinct T cell subpopulations are being evaluated for their ability to activate monokine production and cytostatic activity in the macrophage population and to become activated to produce lymphokines. The role of cognate and non-cognate T cell-macrophage interactions in inducing these effector functions and in amplifying cellular immune reactions are being investigated.

Key facts

NIH application ID
3176543
Project number
5R01CA038408-05
Recipient
EAST TENNESSEE STATE UNIVERSITY
SAM.gov UEI
V5LLVC627U34
Principal Investigator
ROBERT D STOUT
Activity code
R01
Funding institute
NIH
Fiscal year
1989
Award amount
$85,723
Award type
5
Project period
1983-12-01 → 1991-03-31