# PDGF EFFECTS ON T-CELL BEHAVIOR IN AGING

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1993 · $181,452

## Abstract

We recently made the novel discovery that platelet derived growth factor
(PDGF) is capable of profoundly altering the responsiveness of murine T
cells, through its capacity to control the species and patterns of
lymphokines produced following cellular activation.  this finding takes
on a significant degree of importance, when one considers that most
experimentalists in immunology, who utilize in vitro procedures in their
research, routinely employ some source of serum as a culture medium
supplement.  Serum, unlike plasma, is heavily contaminated by a number
of biologically active growth factors (including PDGF) as a consequence
of blood clotting and the resultant platelet activation.  By considering
the types of T cell responses controlled by PDGF, and the duration of
this regulatory influence prior to growth factor desensitization, some
of the reported "differentiation" events that occur in vitro following
cellular activation under serum containing conditions are easily
explained.  Maybe these model systems, some of which represent presently
accepted paradigms, will have to now be restructured.  We have chosen to
look beyond the effects of PDGF, as a creator of biologic artifacts on
T cell function in vitro.  Our present studies investigate the in vivo
role(s) played by this growth factor in orchestrating the potential of
T cells to respond under special sets of circumstances.  As will become
apparent from the data presented, PDGF could be playing a central,
although totally overlooked, role in controlling mammalian immune
responses in vivo.  This regulatory system is proving to be beautifully
complex, and involves both active and antagonistic PDGF isoforms.  Also
important to the system is a requirement for cell surface expression of
both alpha- and beta-type receptor subunits for T cell responsiveness.
T cells isolated from gut mucosa draining lymphoid organs of normal
murine donors were found to lack responsiveness to the effects of  PDGF,
and PDGF responsiveness is totally lost as a consequence of old age.
Both of these phenomena appear to be directly linked to activities
mediated by the cytokine IL-6.  IL-6 may be produced locally in gut-
mucosa draining lymphoid compartments.  We have recently discovered that
control over the production of IL-6 is dysregulated as a consequence of
normal aging, a finding which possesses significant biologic and
immunobiologic importance.  The experimental plan presented herein is
purposefully comprehensive, and includes an analysis of PDGF-influences
on cytokine production by human T cells.  We will investigate PDGF
isoform dependence, receptor subunit requirements, the modulatory
influence by IL-6, and the effect of donor age on growth factor
responsiveness.  Also included in this proposal, is a research plan to
advance our understanding of the murine system.  Studies to investigate
T cell subset responsiveness, dependence on lymphoid organ source, the
effects of T cell donor age and its relationship to dy...

## Key facts

- **NIH application ID:** 3123401
- **Project number:** 1R01AG011475-01
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** RAYMOND A DAYNES
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $181,452
- **Award type:** 1
- **Project period:** 1993-04-01 → 1997-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3123401

## Citation

> US National Institutes of Health, RePORTER application 3123401, PDGF EFFECTS ON T-CELL BEHAVIOR IN AGING (1R01AG011475-01). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3123401. Licensed CC0.

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