# AUTOANTIBODIES TO ACTIVATED LYMPHOCYTES IN SLE

> **NIH NIH R01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 1988 · $208,547

## Abstract

Systemic lupus erythematosus (SLE) is a chronic multisystem
disease characterized by a variety of immunological
abnormalities, and has become a prototype for study of
autoimmunity and immune complex-mediated tissue injury.
Considerable evidence suggests that different types of
autoantibodies to lymphocytes may be of fundamental importance
with respect to immune system dysfunction in this disorder.
Investigation during the past four years has increased our
understanding of resting and activated T cell target antigen
specificities in this system, and has delineated several interesting
mechanisms by which anti-lymphocyte autoantibodies influence
cell surface antigen expression, T cell populations in the
circulation, and T cell activation.  While broader in scope than the
original application, the overall objective of the present proposal
continues to be the definition of the nature and significance of
anti-lymphocyte autoantibodies in SLE.  Emphasis in Aim I is
placed on the identification and biochemical characterization of
autoantibody target molecules on different cell types.  Special
effort will be made to determine whether anti-lymphocyte
antibody-reactive antigens are carbohydrate in nature become
phosphorylated during T cell activation, and are attached to the
cytoskeleton.  Experiments in Aim II will study anti-lymphocyte
antibodies as activation ligands, and will clarify the mechanism(s)
by which they inhibit T cell activation.  Aim III concerns the
relationship of anti-lymphocyte autoantibodies with clinical
disease expression and the natural history of SLE.  Lymphocytes
and serum obtained from patients at different points in their
illness, or with clinically distinct manifestations, will be analyzed
in comparative immunofluorescence/cytotoxicity and Western
blotting experiments.  Also of interest in this aim are experiments
to determine whether in vivo T cell subset depletion and
endogenous T cell activation contribute to hypoproliferation in
vitro.  Autoantibodies and monoclonal antibodies which cross-
react with cellular constituents from nuclear, cytoplasmic and
plasma membrane compartments will be used in Aim IV to search
for homologous epitopes shared by membrane surface targets of
anti-lymphocyte autoantibodies.  Cross-reactive idiotypes and
light chain restriction of anti-lymphocyte antibody Ig will be
sought as well.  Anti-lymphocyte antibodies in patients with virus
infections and non-SLE auto-immune diseases will be studied in
Aim V to provide clues, vis a vis molecular mimicry (epitope
homology), regarding putative microbial triggers of SLE and
related disorders.

## Key facts

- **NIH application ID:** 3155908
- **Project number:** 5R01AR030863-07
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **SAM.gov UEI:** D3LHU66KBLD5
- **Principal Investigator:** JOHN B WINFIELD
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $208,547
- **Award type:** 5
- **Project period:** 1982-04-01 → 1992-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155908

## Citation

> US National Institutes of Health, RePORTER application 3155908, AUTOANTIBODIES TO ACTIVATED LYMPHOCYTES IN SLE (5R01AR030863-07). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3155908. Licensed CC0.

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