# B CELL HYPERACTIVITY IN AUTOIMMUNITY

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CAMPUS · 1987 · $59,691

## Abstract

The purpose of the proposed study is to delineate the basic
immunological defects responsible for B cell hyperactivity in
MRL/1 autoimmune mice.  Three specific issues will be
addressed:  (1) In order to identify the intrinsic immune
defect(s) resulting in excessive B cell activity, "autoimmune x
normal" chmieric mice will be produced in which T cells and B
cells derived from a mixture of normal and auto-immune stem
cells mature together in an autoimmune environment.  The
strains selected for the study differ with respect to their
Thy-1 and Igh allotype markers such that it will be possible to
monitor the extent and source (normal or autoimmune parent) of
B cell antibody production as well as T cell lymphokine
production; (2) To clarify the relationship between non-self
antigen induced responses and autoantibody production,
autoimmune mice capable of making a hapten specific
cross-reactive idiotype (CRI) will be immunized with
hapten-protein conjugates and screened periodically for
expression of the CRI-associated VHDHJH in the polyclonally
activated B cell pool; (3) To examine the role of autologous
antigen in inducing an autoimmune response, backcross mice
derived from mating autoimmune with normal mice will be
produced and allotype specificity of rheumatoid factors derived
from the Igh homozygous mice will be compared to the allotype
specificity of rheumatoid factors derived from the Igh
heterozygous mice.  The autoimmune Igh heterozygous mice will
also be used to look for possible linkage between anti-IgG
binding specificities and the igh haplotype of the autoimmune
parent.  Overall these studies should contribute to our basic
understanding of the mechanisms regulating B cell activation
and antibody production.  The results of this proposal should
eventually have clinical application with regard to the control
of the basic immunoregulatory defects involved in autoimmune
disorders such as systemic lupus erythematosus and rheumatoid
arthritis as well as certain forms of graft-versus-host disease.

## Key facts

- **NIH application ID:** 3157120
- **Project number:** 5R01AR035230-02
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CAMPUS
- **SAM.gov UEI:** FBYMGMHW4X95
- **Principal Investigator:** Ann Marshak-Rothstein
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $59,691
- **Award type:** 5
- **Project period:** 1986-09-22 → 1989-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157120

## Citation

> US National Institutes of Health, RePORTER application 3157120, B CELL HYPERACTIVITY IN AUTOIMMUNITY (5R01AR035230-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157120. Licensed CC0.

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