# T CELL FIBRONECTIN

> **NIH NIH R01** · NEW YORK MEDICAL COLLEGE · 1992 · $234,300

## Abstract

Alterations in cellular immunity and cytokine (lymphokine) production are
features of many human diseases, both neoplastic and non-neoplastic.
Therapeutic manipulation of this important element of the immune response
requires a more complete biochemical understanding of cytokine structure
and function than is currently available.  T cell fibronectin (FN), a
lymphokine produced by antigen and mitogen activated T ells, is involved in
the initiation of delayed hypersensitivity inflammatory reactions.  During
the past project period we have found that monoclonal antibodies able to
neutralize the monocyte agglutinating activity of T cell FN in vitro
inhibit the expression of delayed hypersensitivity vascular responses in
vivo.  The FN are a family of closely related, high molecular weight
glycoproteins found in plasma and tissues.  Different FN arise by cell-
specific alternative splicing of mRNA derived from a primary transcript of
a single complex gene.  Although T cell FN shares many properties with
other FN, its distinctly smaller molecular weight and extraordinarily high
activity relative to other cellular FN documented during the past project
period suggests that it differs from them in primary sequence.  The project
is divided into two subprojects.  Subproject 1 will define differences
between T cell and other FN at the primary sequence level.  Segments of T
cell FN cDNA synthesized from T cell FN mRNA by reverse transcriptase will
be amplified by the polymerase chain reaction, and their size compared with
size predicted from the known sequence of the FN gene and observed after
amplification of other cDNA derived from other cellular FN.  Segments
differing in length from the predicted value will be sequenced to determine
which domains are present in T cell FN and how this choice of domains
differs from that seen in other FN.  Subproject 2 will study the mechanism
of action of T cell FN and its interaction with other lymphokines in the
initiation of DH inflammatory reactions.  Studies in vitro will employ a
model based on a two-compartment culture system separated by a confluent
endothelial cell monolayer and assays for T cell FN activities (monocyte
agglutination, matrix-driven translocation).  Lymphokines, vasodilating
arachidonic acid metabolites, peptides based on T cell FN sequences and
expressed sequences of T cell FN (from materials generated in subproject 1)
that are able to modify release of T cell FN or its activities in vitro
will be studied for their effects on in vivo delayed hypersensitivity
reactions in order to clarify the role of T cell FN in these cellular
immune reactions.

## Key facts

- **NIH application ID:** 3171895
- **Project number:** 2R01CA034141-11
- **Recipient organization:** NEW YORK MEDICAL COLLEGE
- **SAM.gov UEI:** WK63UJ11C2H7
- **Principal Investigator:** HENRY Philip GODFREY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $234,300
- **Award type:** 2
- **Project period:** 1982-07-01 → 1995-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171895

## Citation

> US National Institutes of Health, RePORTER application 3171895, T CELL FIBRONECTIN (2R01CA034141-11). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171895. Licensed CC0.

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