# NEW CUTANEOUS MODEL OF GRANULOMATOUS INFLAMMATION

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 1990 · $186,991

## Abstract

The long range plan of this research project is to understand the
pathomechanisms of human cutaneous hypersensitivity
granulomas, such as sarcoidosis, metal-induced granulomas and
tuberculoid leprosy.  These diseases create a disabling and
crippling condition in patients, and because of a lack of
information about the disease process patients do not receive
adequate treatment.  A new cutaneous model for granulomatous
disease has been developed which closely mimics human skin
granulomas.  It will be used to probe basic pathomechanisms and
fill gaps in our knowledge.  The hypothesis t be tested proposes
that hypersensitivity granulomas evolve from two overlapping and
perhaps interdependent events, an initiation event which is
independent of the T-cell mediated immune system and promotion
event which embodies T-cell mechanisms to expand the
efflorescence of clinically apparent granulomas.  Using athymic
and euthymic littermates, direct experiments are planned to
demonstrate that 1) granulomas can be initiated without eliciting
evidence of T-cell maturation or function and 2) the initiated
granulomatous reaction can be expanded by T-cell functions in
euthymic mice and by supplementation of T-cell functions in
athymic mice.  Furthermore, we will attempt to biochemically
characterize both granuloma "initiating" and "promoting" factors.

Because there is a need to biochemically distinguish
hypersensitivity granulomas from chronic inflammation and
foreign body reactions in skin, additional effort will be directed to
test some recently described enzymes from activated
macrophages in the cutaneous model to better define organized
granulomatous inflammation in biochemical terms.  It has been
recognized that biochemical properties of granulomas in skin may
differ from granulomatous lesions in other body sites.

In earlier studies eosinophilia along with granuloma formation
were transferred by viable cells from euthymic mice to both
athymic and euthymic mice.  "Eosinophilia transfer factor" which
becomes inactive by freeze-drying will be separately isolated
from fresh granulomas.

It is expected that the findings from the project will provide
information about how organized epithelioid cell granulomas are
formed in skin and will offer a more cohesive view of the total
disease process.

## Key facts

- **NIH application ID:** 3156125
- **Project number:** 5R01AR031853-07
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **SAM.gov UEI:** KMH5K9V7S518
- **Principal Investigator:** WILLIAM L EPSTEIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $186,991
- **Award type:** 5
- **Project period:** 1983-02-01 → 1992-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156125

## Citation

> US National Institutes of Health, RePORTER application 3156125, NEW CUTANEOUS MODEL OF GRANULOMATOUS INFLAMMATION (5R01AR031853-07). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3156125. Licensed CC0.

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