# MECHANISMS OF CUTANEOUS INJURY IN LUPUS ERYTHEMATOSUS

> **NIH NIH R01** · UT SOUTHWESTERN MEDICAL CENTER · 1989 · $150,674

## Abstract

We will test our hypothesis that lupus erythematosus (LE)-specific skin
injury results from a humoral and/or cell-mediated immune response that is
directed toward auto- or neo-antigens present in the epidermis or at the
(D-E) dermal-epidermal junction.  A key to better understanding the
pathogenetic basis of this highly characteristic cutaneous injury pattern
lies in identifying those auto-/neo-antigens and better characterizing the
immune response which is directed toward them.  Such studies could yield
both the tools and strategies necessary for developing in vitro and in vivo
models of this histopathological reaction.  Our specific aims for achieving
these goals are:  1) To further characterize Ro/SS-A and the autoimmune
response which occurs to this antigen.  2) To identify and isolate other
cutaneous auto-/neo-antigens relevant to the expression of cutaneous LE.
3) To develop human T-cell clones from LE-specific skin lesions which could
then be used to probe for cutaneous LE-relevant auto-/neo-antigens and to
develop a human in vitro model of the cutaneous LE histopathological
reaction.  4) To develop an animal model of cutaneous LE utilizing T-cell
clones which exhibit epidermal or D-E junctional auto-/neo-antigen
specificity.  5) To characterize further the pathogenetic mechanism(s)
involved in the photosensitivity exhibited by some cutaneous LE patients.
6) To characterize further the immunoregulatory disorders present in
cutaneous LE patients.  7) to identify additional risk factors for severe
SLE in subacute cutaneous lupus erythematosus patients.  It has long been
our feeling that a better understanding of the pathogenesis of cutaneous LE
could yield not only significant improvement in the clinical management of
this aspect of the disease, but might also furnish new insight into the
etiology of the LE tissue injury mechanisms which occur in less accessible
target organs such as the kidney and central nervous system and large
vessels.  These studies might also yield insight into the pathogenesis of
other related inflammatory skin diseases such as lichen planus,
dermatomyositis and lichenoid drug eruptions.

## Key facts

- **NIH application ID:** 3155030
- **Project number:** 5R01AR019101-13
- **Recipient organization:** UT SOUTHWESTERN MEDICAL CENTER
- **SAM.gov UEI:** YZJ6DKPM4W63
- **Principal Investigator:** Richard Dennis Sontheimer
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $150,674
- **Award type:** 5
- **Project period:** 1979-05-01 → 1989-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155030

## Citation

> US National Institutes of Health, RePORTER application 3155030, MECHANISMS OF CUTANEOUS INJURY IN LUPUS ERYTHEMATOSUS (5R01AR019101-13). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3155030. Licensed CC0.

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