# ANTI-IDIOTYPIC CONTROL OF NEURAL AND ALLERGIC DISEASES

> **NIH NIH R01** · YALE UNIVERSITY · 1988 · $158,016

## Abstract

Experimental autoimmune myasthenia gravis (EAMG) has been
produced in C57BL/6 mice by immunization with torpedo acetyl
choline receptor.  Our laboratory has developed suppressor T cell
lines and clones derived from lymph node cells of immunized
animals.  The present proposal concerns three phases.  The first
two have to do with enriching T cell lines for both helper and
suppressor activity and hybridizing these lines to form
immortalized T cell hybridomas.  Our method will be to induce
suppressor T cells by a variety of means including antigen coupled
cells, and by pretreating the animals with total lymphoid
irradiation.  Cells from animals in whom suppressor cells have
been induced will be enriched by both panning and rosetting means
prior to hybridization.  Finally, T cells will be hybridized and
selected for the capacity to suppress lymph node cell proliferation
of immunized lymph node cells, and to suppress antibody
production in vitro and delayed type hypersensitivity as measured
both by ear swelling and footpad swelling.  The production of
helper T cell hybrids will be used to facilitate study of the
potential augmentation of the development of experimental
autoimmune myasthenia gravis in mouse strains.  If transfer of
helper hybrids induces the disease in susceptible strains, then
means of attenuation of such hybrids with chemical, drug or X-ray
are contemplated.

A major new thrust of the present proposal is the study of
network induced myasthenic syndrome.  In this syndrome
weakness is induced by immunization of animals with the idiotypic
antibodies produced by ligands of the acetylcholine receptor.  This
syndrome is, in many respects, closer to the model of human
disease then is that produced in experimental autoimmune
myasthenia after immunizing animals with the torpedo acetyl
choline receptor.  Two ligands will be used to study this system:
siamese cobra neurotoxin, and anti-AChR antibodies.  In both the
parts of this proposal our use of the network is to understand
natural regulatory factors in the immune system leading to the
development of clinical myasthenia and thereby hoping to
modulate these factors.

We have recently been successful in immunizing mice and
producing EAMG with a 32 amino-acid oligopeptide of the
acetylcholine receptor.  This peptide will now be studied as an
inducer of suppressor cells, helper cells, and as a toleragen.

## Key facts

- **NIH application ID:** 3127409
- **Project number:** 5R01AI017716-08
- **Recipient organization:** YALE UNIVERSITY
- **SAM.gov UEI:** FL6GV84CKN57
- **Principal Investigator:** FRED S KANTOR
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $158,016
- **Award type:** 5
- **Project period:** 1987-09-30 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127409

## Citation

> US National Institutes of Health, RePORTER application 3127409, ANTI-IDIOTYPIC CONTROL OF NEURAL AND ALLERGIC DISEASES (5R01AI017716-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3127409. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*