# RHEUMATOID FACTORS IN AUTOIMMUNE MODEL

> **NIH NIH R01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 1987 · $82,318

## Abstract

Rheumatoid factors (RF, anti-IgG) are important in the pathophysiology of
human autoimmune diseases such as rheumatoid arthritis (RA) and systemic
lupus erythematosus (SLE).  The specificities and idiotypes of these
rheumatoid factors may be relevant to their pathogenic potential in
autoimmune diseases, since human RFs in nonrheumatoid conditions appear to
have different specificities.  Theoretically, rheumatoid factors could
develop as a response to a specific autoimmunogenic stimulus, polyclonal
activation, or to altered homologous IgG or immune complexes.  These
stimuli might trigger different immunoregulatory mechanisms.
Unfortunately, experimental systems where such isolated, defined stimuli
can be applied are uncommon.  For example, though RF titers correlate with
arthritis in the MRL-1pr/1pr mouse strain, analysis is confounded by the
fact that the congenic MRL line is also autoimmune.

In the proposed experiments, anti-IgG spontaneously produced in B6-1pr/1pr
and normal non-autoimmune B6-+/+ mice will be characterized.  Anti-IgG will
also be induced by mitogenic and chronic antigenic stimulation and by
immunization with altered IgGs.  RF activity will be characterized by
quantity, specificity, and idiotype.  Preliminary studies strongly suggest
that the anti-IgG specificities occurring spontaneously in the B6-1pr/1pr
female are distinct from those of the B6-1pr/1pr male and anti-IgGs
inducible or occurring spontaneously in normal B6 mice.  Significant RF
clonotypes will be identified by specificity and isoelectric focusing, and
hybridomas initially isolated by specificity.  Anti-idiotypic reagents will
then be utilized to investigate the RF idiotypic representation in sera of
other 1pr and their respective parent congenic strains.  These reagents
will also be used in the study of the in vitro production of RF, in which
the cellular requirements and sources for the production of various RF
idiotypes and specificities will be defined.  These results should provide
clues to the mechanism of rheumatoid factor production in human autoimmune
disease.

## Key facts

- **NIH application ID:** 3156765
- **Project number:** 5R01AR034253-03
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **SAM.gov UEI:** D3LHU66KBLD5
- **Principal Investigator:** ROBERT W WARREN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $82,318
- **Award type:** 5
- **Project period:** 1985-07-01 → 1988-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156765

## Citation

> US National Institutes of Health, RePORTER application 3156765, RHEUMATOID FACTORS IN AUTOIMMUNE MODEL (5R01AR034253-03). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3156765. Licensed CC0.

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