# REGULATION OF HUMAN IGE IN HEALTH AND DISEASE

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 1987 · $153,282

## Abstract

This proposal will primarily examine the cellular events regulating the
production of human allergic (IgE) antibodies utilizing two newly defined
in vitro systems of human IgE synthesis.  We have developed and in vitro
analogue of ongoing IgE synthesis employing mycoplasma free clones of IgE
secreting cells recently derived by us from the human IgE plasma cell line,
U266.  The clones are responsive to both inhibitory (suppressor cells and
supernatants) and helper (T cell IgE enhancing factor) activities and thus
allow us to assay both positive and negative aspects of IgE regulation.  By
employing IgA and IgG secreting cells in the same wells, we will assess
isotype specific effects.  This will be complemented by induction of IgE
synthesis from resting human B cells using IgE enhancing factor derived
from cultured T cells from patients with high levels of IgE.  Thus we will
examine both regulation of induction as well as ongoing IgE production.
Particular emphasis will be given to the role of IgE in regulation of both
B and T cells through use of defined Ige anti-IgE immune complexes.  These
complexes will be constructed from purified human IgE and mouse monoclonal
anti Fc epsilon (FcEpsilon) antibodies which have been produced and well
characterized by us.  Data with these complexes shows isotype specific
effects on both IgE regulatory T cells and producing B cells.  Differential
effects on T cell expression of IgE regulatory activities induced by the
nature of IgE complex binding (i.e. alone or in the presence of antigen)
will be tested.  Expression of the FcE receptor will be assessed by our
newly perfected technique whereby IgE anti-IgE complexes are bound to cells
and then detected via immunoperoxidase staining.  We will probe the
relationship between FcE and Fc gamma receptor expression on T cells and
their regulation of IgE.  Further functional evaluation of the various
cells will be achieved by enriching the cells according to their isotype Fc
receptors.  Regulatory IgE cells will be expanded for in-depth study by
Interleukon II and T cell clones derived using HTLV II transformation.  The
expression on IgE committed B cells of FcE receptors as potential acceptor
sites for complexes of IgE-IgE binding regulatory factors will also be
explored.  These studies will be extended to the cells from patients
already demonstrated to have abberant control of IgE.  Seleted molecular
studies will be undertaken to extend the cellular results as to the
mechanisms of regulatory events at the B cell level.

## Key facts

- **NIH application ID:** 3126106
- **Project number:** 5R01AI015251-09
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **SAM.gov UEI:** RN64EPNH8JC6
- **Principal Investigator:** ANDREW SAXON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $153,282
- **Award type:** 5
- **Project period:** 1978-08-01 → 1988-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126106

## Citation

> US National Institutes of Health, RePORTER application 3126106, REGULATION OF HUMAN IGE IN HEALTH AND DISEASE (5R01AI015251-09). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126106. Licensed CC0.

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