# B CELL ACTIVATION IN AUTOIMMUNITY & LYMPHOPROLIFERATION

> **NIH NIH R01** · SCRIPPS CLINIC AND RESEARCH FOUNDATION · 1987 · $137,178

## Abstract

A variety of immunologic, virologic, hormonal, and genetic abnormalities
have been catalogued in murine strains with with systemic lupus
erythematosus (SLE)-like syndromes.  However, no common link or molecular
basis for such abnormalities has yet been identified.  Among the various
abnormalities, B cell hyperactivity leading to autoantibody production is
the common and cardinal feature of all SLE murine strains, as well as of
humans with SLE.  Whether this B cell abnormality is primary or secondary
to helper or suppresor T cell defects remains controversial and and unclear
at the present.

A large body of recent work indicates that proliferative and
differentiative events in B and T cell development are induced by a cascade
of antigen-specific and nonspecific soluble mediators elaborated by
activated T cells, macrophages, and perhaps other elements of the immune
systems.  In order to clarify further the essential immunologic
abnormalities that lead to autoimmune disorders and perhaps devise means
for their molecular analysis, we propose to:  (a) measure the effects of
soluble T cell-derived factors with known activities on B cells of SLE and
normal control murine strains; (b) assess the in vitro elaboration of
soluble mediators by limphoid cells of SLE and control strains that might
influence B cell differentiative and muturational processes and, if
identified, determine their levels, cellular origin, mode of action, and
relationship to the disease state:  (c) isolate and biochemically
characterize the factos, attempt to produce antibodies against them and
subsequently assess the in vitro and in vivo effects of the factors and of
respective antibodies; and (d) develop new lines of SLE mice defective in
expression of acceptor sites for T cell-derived signals so as to ascertain
the in vivo importance of the factors and of the target cell component in
disease expression.  These studies will clarify the means of B cell
activation in systemic autoimmune diseases, provide further understanding
of the interplay among lymphokines that participate in cellular and humoral
immune responses, and may allow, in the future, molecular analysis and
modification of this and related disorders.

## Key facts

- **NIH application ID:** 3156656
- **Project number:** 5R01AR033826-04
- **Recipient organization:** SCRIPPS CLINIC AND RESEARCH FOUNDATION
- **Principal Investigator:** Argyrios N Theofilopoulos
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $137,178
- **Award type:** 5
- **Project period:** 1984-06-01 → 1989-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156656

## Citation

> US National Institutes of Health, RePORTER application 3156656, B CELL ACTIVATION IN AUTOIMMUNITY & LYMPHOPROLIFERATION (5R01AR033826-04). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3156656. Licensed CC0.

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