# PEMPHIGUS AND PEMPHIGOID

> **NIH NIH R01** · MEDICAL COLLEGE OF WISCONSIN · 1989 · $218,033

## Abstract

The human dermatological diseases pemphigus and pemphigoid are true
autoimmune disorders in which patients become sensitizied to epidermal
antigens, producing autoantibodies which in turn are rsponsible for the
severe blistering eruption that occurs in the skin.

This competitive renewal application represents a collection of ongoing
research projects that started several years ago.  The highlights of these
studies, listed in the progress report, include the development of the
first animal models for pemphigus and pemphigoid, studies on the evolution
of the epidermal lesions that are induced in the pemphigus animal model,
studies on the fate of pemphigus antibodies after binding the keratinocyte
cell surface in vitro, the localization of pemphigoid antigen in the
epidermal basal cell hemidesmosome-cytoskeleton complex and the development
of hybridomas that secrete antibodies with specificity for the
epidermal-dermal junction that is similar to human pemphigoid
autoantibodies antibodies by immunofluorescene criteria.

This application describes studies which will a) define the role of
keratinocyte surface cross-linking, complement, and neutrophils in the
pathogenesis of pemphigus scantholysis in vivo, b) further define the
nature of pemphigoid antigen which is currently partially purified, and c)
continue the cloning and characterization of the pemphigoid monoclonal
antibodies referred to above.  In the present application, we also include
sections dealing with the purification of pemphigus antigens and the
development of monoclonal antibodies against these antigens using unique
approaches, i.e., the human-human system.

At the end of the funding period we anticipate that we will have: (a) a
pure, highly specific marker of basal cell hemidesosomes, i.e., the
pemphigoid antigen as defined by the human autoantibodies and our
monoclonal antibodies, (b) a pure, and highly specific keratinocyte cell
surface marker, i.e., the pemphigus antigen and its corresponding human
autoantibodies and monoclonal antibodies, and (c) a better understanding of
the molecular mechanisms by which pemphigus autoantibodies trigger
acentholysis in vivo.

## Key facts

- **NIH application ID:** 3156187
- **Project number:** 5R01AR032081-08
- **Recipient organization:** MEDICAL COLLEGE OF WISCONSIN
- **SAM.gov UEI:** E8VWJXMMUQ67
- **Principal Investigator:** Luis A. Diaz
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $218,033
- **Award type:** 5
- **Project period:** 1988-07-01 → 1990-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156187

## Citation

> US National Institutes of Health, RePORTER application 3156187, PEMPHIGUS AND PEMPHIGOID (5R01AR032081-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3156187. Licensed CC0.

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