# AUTO-REACTIVE T LYMPHOCYTES, LEUKOKINES, AND COLLAGEN

> **NIH NIH R01** · CHILDREN'S HOSPITAL OF LOS ANGELES · 1988 · $121,930

## Abstract

Increased collagen deposition is a clinical and
histopathological feature of many rheumatoid and inflammatory
diseases.  Most evidence indicates that the collagen deposition
is due to increased fibroblast collagen production secondary to
leukokine stimulation.  However, evaluation of the leukokine
control of fibroblast collagen production has been limited by
the lack of defined systems.  Chronic graft versus host disease
(cGVHD) produced by the bone marrow transplantation of H-2
identical, non-H-2 non-identical mice is a model system of
increased collagen deposition.  Using this model system we have
identified two populations of T lymphocyte clones that control
fibroblast collagen production through separate leukokines.
One population of T lymphocytes produces a leukokine that
stimulates fibroblast proliferation whereas the other
population of T lymphocytes produces a leukokine that
stimulates fibroblast collagen synthesis on a per cell basis.
The clones that stimulate per cell collagen synthesis have
specificity for autologous I-A.  Since auto-reactive T
lymphocytes are normally present in mice and humans, they may
under appropriate circumstances produce leukokines that
stimulate collagen production.  To determine if naturally
occurring autoreactive T lymphocytes produce collagen
stimulating leukokines, T lymphocyte clones will be generated
from autologous mixed lymphocyte reaction (AMLR) stimulated by
non-T lymphocytes, activated T lymphocytes, and I-A positive
fibroblasts and will be assayed for the production of collagen
stimulating leukokines.  Since clinically increased collagen
deposition is anatomically localized, the localization may be
due to tissue specific differences in the fibroblast
responses.  The expression of I-A by fibroblasts is found in a
variety of disease states.  The role of fibroblast I-A in the
stimulation of the auto-reactive, I-A specific T lymphocytes
will be determined.  The mechanism of action of the collagen
stimulating leukokines will be determined.  In summary, the
role of auto-reactive T lymphocytes and their leukokines in the
control of fibroblast collagen production will be studied in a
model system.

## Key facts

- **NIH application ID:** 3158104
- **Project number:** 5R01AR037394-03
- **Recipient organization:** CHILDREN'S HOSPITAL OF LOS ANGELES
- **SAM.gov UEI:** DVL1CMRMWRN9
- **Principal Investigator:** Robertson Parkman
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $121,930
- **Award type:** 5
- **Project period:** 1986-07-01 → 1989-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3158104

## Citation

> US National Institutes of Health, RePORTER application 3158104, AUTO-REACTIVE T LYMPHOCYTES, LEUKOKINES, AND COLLAGEN (5R01AR037394-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3158104. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*