# IMMUNOLOGY MECHANISM OF ANAPHYLAXIS

> **NIH NIH R01** · NEW YORK UNIVERSITY · 1991 · $154,204

## Abstract

DESCRIPTION (Adapted from the applicant's abstract):  Two groups of
experiments are planned.  These problems are interconnected as both concern
the murine IgE molecule.  The first goal of this proposal is to continue
studies of the production of anti-dinitrophenyl (DNP) IgE antibody and the
influence of interleukins, especially IL-4, on the switch from IgM
production to anti-DNP IgE production.  Most of the previous work,
published by several authors, investigated the switch from "normal"
polyclonal immunoglobulins of the IgM or IgG classes to polyclonal "normal"
IgE.  The word "normal" underlines that fact that the specificity of the
immunoglobulins, the antigen with which they react, is unknown.  Two T
helper cell clones (L3T4) will be used.  These clones are specific for
keyhole limpet hemocyanin (KLH) and both were already investigated using B
cells primed for anti-DNP antibody production.  The production of anti-DNP
IgM and IgG were both investigated, but not the production of anti-DNP IgE.
These clones will be used together with B cells from mice syngeneic to the
T cell clones.  The influence of recombinant interleukins rIL-4 and rIL-2,
and the influence of monoclonal anti-IL-4 and anti-IL-2 on anti-DNP IgE
production will be investigated.

The second goal is to study the in vitro suppression of IgE antibody
specific for the DNP (dinitrophenyl) hapten.  Using adoptive transfer, the
applicant has demonstrated that in the SJL strain of mice, suppression of
IgE antibody against DNP can be obtained.  Mice primed with DNP-protein and
given T cells from other mice that have been hyperprimed with an unrelated
carrier protein suppress anti-DNP IgE production if this second carrier is
injected.  Dr. Ovary proposes to study this suppression in vitro and then
instead of using hyperprimed spleen cells (plus antigen) study the possible
suppressive affects in this system of different lymphokines.  If
successful, he proposes to use the system described above (first goal) to
examine suppression of antigen specific IgE when well-defined cloned T
cells are used as helper cells.

## Key facts

- **NIH application ID:** 3124118
- **Project number:** 2R01AI003075-30A3
- **Recipient organization:** NEW YORK UNIVERSITY
- **SAM.gov UEI:** NX9PXMKW5KW8
- **Principal Investigator:** ZOLTAN OVARY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $154,204
- **Award type:** 2
- **Project period:** 1974-12-01 → 1994-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124118

## Citation

> US National Institutes of Health, RePORTER application 3124118, IMMUNOLOGY MECHANISM OF ANAPHYLAXIS (2R01AI003075-30A3). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124118. Licensed CC0.

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