# MEDIATOR OF CELLULAR IMMUNITY

> **NIH NIH R01** · CORNELL UNIVERSITY · 1988 · $170,402

## Abstract

Cellular events underlying the expression of resistance to Listeria
monocytogenes (LM) would be analyzed in a model system using rats.  Central
to the proposed inquiry is the relationship between delayed type
hypersensitivity (DTH) and acquired cellular resistance to infection
(CRI).  These two phenomena are mediated by T cells which have distinctive
phenotypic characteristics, gene constraints, and possibly different
lymphokine repertoires.  But the two major subsets to which TDTH and TCRI
belong are themselves heterogeneous.  Each contain cells that have
distinctive surface antigenic profiles and functional properties.  A major
objective of the proposed investigation is to systematically define these
subsets and to ascertain the capacity of their component cells to interact
with one another and with macrophages.  To that end monoclonal antibodies,
panning techniques and both new and established methods of flow cytometry
would be used to isolate T cell subsets from the central lymph of LM
infected rats.  Using sensitive and reproducible assays we would ascertain
the effective life span of the cells, their tissue disposition in recipient
rats, gene restriction, and capacity to influence the local deployment of T
cells and macrophages in DTH reaction sites and centers of infection.  The
above findings would be correlated with the lymphokine repertoire of subset
defined T cells and their capacity to influence the microbicidal activity
of macrophages.  Subsidiary questions to be addressed include the role of
suppressor T cells (Ts) in regulating the production of TDTH and TCRI;
whether the sensitivity elicited by living LM involves the activity of
additional or possibly different TDTH from those engaged by soluble
Listeria antigens or killed bacteria; and whether relevant T cell subsets
can be engaged selectively by altering the immunization strategy in various
ways.  Still another aspect of the proposed investigation would focus on a
critical early event in the delayed inflammatory reaction.  We wish to test
the proposition that fibronectin (FN) functions as a ligand between
recently activated T cells and inflamed vascular endothelium; the type(s)
of FN and T cells involved, and whether that interaction can be modified in
useful ways.

## Key facts

- **NIH application ID:** 3125757
- **Project number:** 5R01AI014482-11
- **Recipient organization:** CORNELL UNIVERSITY
- **SAM.gov UEI:** G56PUALJ3KT5
- **Principal Investigator:** DOUGLAS D MCGREGOR
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $170,402
- **Award type:** 5
- **Project period:** 1977-05-01 → 1990-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125757

## Citation

> US National Institutes of Health, RePORTER application 3125757, MEDIATOR OF CELLULAR IMMUNITY (5R01AI014482-11). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125757. Licensed CC0.

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