# RHEUMATIC DISEASE:  IMMUNE COMPLEXES & IMMUNOGENETICS

> **NIH NIH R01** · BRIGHAM AND WOMEN'S HOSPITAL · 1987 · $134,942

## Abstract

The specific aims of this study is to elucidate the role of immune
complexes, complement, immune cells, and genetic factors in patients with
rheumatic and related diseases, particularly SLE.  The frequency of
histocompatibility antigens (HLA) and other genetic markers (complement
allotypes, Gm, red cell C3b receptors) in patients, relatives, and normals
will be determined in order to better define the genetic susceptibility of
individuals to disease.  This definition will be expanded and enhanced by
determining associations between these genetic markers and the clinical
features and immunological abnormalities in these patients.
Genetic-disease associations will then be further characterized by
defining, at the cellular level, how these genetic factors influence the
induction of these immune abnormalities in vitro.  Specifically,
mononuclear cells from genetically defined individuals will be stimulated
with DNA, Sm, RNP, Ro, La, and PWM and specific ANA (i.e., anti-DNA, Sm,
RNP, Ro, and La) produced and quantitated by hemolytic plaque assays and
enzyme-immunoassay (EIA) in the supernatant.  The role of different cells
in this system will be defined by removing monocytes and T-cell subsets and
reconstituting with cells from autologous or genetically identical/similar
(primarily at the Dr loci) patients, relatives, and normals.  Using the
technique developed for the in vitro production of anti-DNA, we plan to
determine whether cells making these antibodies can be selectively killed
utilizing complexes of DNA-poly-L-lysine-ricin.  Successful elimination of
these cells would lead to similar studies in lupus mice to reduce both
anti-DNA antibody titer and immunopathology and would prompt similar
studies in patients.  These studies should improve our understanding of
interrelationships among clinical, immunological, cellular, and genetic
factors in patients with SLE to provide a better framework for management.
Ablation of anti-DNA antibodies may provide a better treatment method in
the short-term.  In the distant future, correction of genetic abnormalities
may be feasible--for now, we must define them.

## Key facts

- **NIH application ID:** 3157879
- **Project number:** 5R01AR037005-03
- **Recipient organization:** BRIGHAM AND WOMEN'S HOSPITAL
- **SAM.gov UEI:** QN6MS4VN7BD1
- **Principal Investigator:** PETER H SCHUR
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $134,942
- **Award type:** 5
- **Project period:** 1985-09-01 → 1988-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157879

## Citation

> US National Institutes of Health, RePORTER application 3157879, RHEUMATIC DISEASE:  IMMUNE COMPLEXES & IMMUNOGENETICS (5R01AR037005-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157879. Licensed CC0.

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