# IMMUNOREGULATION VIA IDIOTYPE NETWORKS

> **NIH NIH R01** · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · 1988 · $114,252

## Abstract

The overall objective of these studies is to determine the structural
character of idiotype(id)-anti-id networks and establish their influence on
normal immune responses.  Studies will utilize as models the two
cross-reactive id(CRI) families (5AF6 and 3C6) assocated with the BALB/c
antibody response against the p-azophenylarsonate-(Ar) hapten.  Sepcific
aims are: (1) to determine the Id expression of early in vivo
antigen-driven anti-Ar Beta cells compared to id produced in vitro by
cloned anti-Ar Beta cells expanded independent of antigen and with id
produced in antigen-driven in vitro cultures.  This will provide an
understanding of id expression and a basis for pursuing Aim #2.  (2) Expand
in vitro and clone anti-id Beta cells derived from normal, id-primed and
antigen-primed BALB/c mice and examine their frequency, specificity, and
influence.  To determine if cloned anti-id Beta cells can recolonize in
vivo and influence normal id expression in response to subsequent antigen
stimulation.  (3) To probe the anti-di repertoire by producing isologous
monoclonal anti-id antibodies specific for the 5AF6 id family dervied from
cloned anti-id Beta cells (Aim #2) and overt immunization with id and
characterize them immunochemically for their specificity, heterogeneity and
their in vivo regulatory influences on id production.  Specific efforts
will be made to stimulate and recover monoclonal anti-id reactive with
idiotopes shared between 5AF6 family anti-Ar and id(+) immunoglobulins(Ig)
not having anti-Ar specificity termed 'parallel id' sets and determine the
regulatory impact of such network related parallel id in normal immune
responses.  Additionally, efforts will be made to elicit, recover, and
characterize monoclonal anti-id that bind id because they bear a variable
region 'internal image' of the Ar hapten.  These studies should establish
the significance of 'parallel id' and 'internal images' in network
immunoregulation.  (4) Contingent on molecular studies, this Aim will
determine the mechanism of depressed 5AF6 and 3C6 id expression associated
with Ig light chain(Vk) and T cell alloantigen(Lyt3)-linked genes.  This is
a novel association between id regulation and these genetic loci.  Together
these aims address fundamental questions of how and to what extent
id-anti-id Beta cell networks influence self regulation of the immune
system.

## Key facts

- **NIH application ID:** 3171849
- **Project number:** 5R01CA034105-06
- **Recipient organization:** ST. JUDE CHILDREN'S RESEARCH HOSPITAL
- **SAM.gov UEI:** JL4JHE9SDRR3
- **Principal Investigator:** ALAN REED BROWN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $114,252
- **Award type:** 5
- **Project period:** 1982-07-01 → 1988-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171849

## Citation

> US National Institutes of Health, RePORTER application 3171849, IMMUNOREGULATION VIA IDIOTYPE NETWORKS (5R01CA034105-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171849. Licensed CC0.

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