# DERMATITIS HERPETIFORMIS - IMMUNOREACTANTS IN THE SKIN

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1987 · $116,878

## Abstract

Dermatitis herpetiformis is a papulovesicular skin disease with an
associated gluten sensitive enteropathy.  Both the skin and bowel disease
improve with gluten restriction.  The skin lesions are characterized by the
accumulation of neutrophils in dermal papillae while immunopathology
reveals IgA and complement in dermal papillae both involved and
"uninvolved" skin.  It has been suggested that cutaneous IgA is directed
against gluten or possibly a cross-reacting antigen in the skin with
complement fixation and subsequent chemotaxis of neutrophils.  This
paradigm of local pathogenesis has been obscured by three basic problems.
1) IgA and complement have been said to be equally distributed throughout
the entire skin, implying that an additional qualitative or quantitative
factor is needed to trigger the inflammatory cascade; 2) Gluten antigen has
not been identified in the skin; 3) The origin, antigenic specificity and
complement binding characteristics of the cutaneous IgA have not been
established.  The last problem is a result of the failure to isolate the
IgA from either the circulation or the skin.  We have hypothesized that:
1) The immunoreactants responsible for chemotaxis (possibly including
gluten, specific complement components, IgA and other immunoglobulins) are
qualitatively or quantitatively unique in or near active lesions.  2)
Clearance of functionally inactive immunoreactants is slow, accounting for
their persistence in previously involved skin (referred to as "uninvolved"
skin by others).  3) Significant amounts of immunoreactants are absent or
markedly decreased in never-involved skin.  4) Isolation of IgA from
preparations of papillary dermis will allow its characterization.

Preliminary data suggest that:

1) IgA is not equally distributed through the entire skin.  2) A relative
quantification of IgA in skin can be accomplished using computerized
analysis of fluorescence.  3) Gluten antigen may be present uniquely in
areas of inflammation.

We plan to test our hypotheses by:  1) obtaining biopsies from
erythematous, previously involved and never-involved skin, 2) obtaining
suction blister fluid from erythematous and previously involved skin, 3)
analyzing skin and blister fluid for immunoglobulin, complement components,
and chemotactic activity, 4) correlating chemotactic activity with
immunoreactant deposition, 5) Lastly, we will isolate IgA from preparations
of papillary dermis using polyacrylamide gel electrophoresis.

## Key facts

- **NIH application ID:** 3157168
- **Project number:** 5R01AR035378-03
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** JOHN J ZONE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $116,878
- **Award type:** 5
- **Project period:** 1985-09-01 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157168

## Citation

> US National Institutes of Health, RePORTER application 3157168, DERMATITIS HERPETIFORMIS - IMMUNOREACTANTS IN THE SKIN (5R01AR035378-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157168. Licensed CC0.

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