# IGE AND IGG SUBCLASS FORMATION

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 1990 · $184,519

## Abstract

Although it is well known that the major cause of allergic diseases is an
overproduction of IgE antibodies, the regulation of IgE antibody
formation is still poorly understood. Recently, it has been shown in both
mice and man that Interleukin-4 (IL-4), a product of T helper cells,
induces B cells to secret IgE. Additionally, IL-4 stimulates murine B
cells to secrete IgG1 and, as shown recently in our laboratory, human B
cells to secrets IgG4. However, the mechanism of human IgE/IgG4 formation
in vitro differs from that in the mouse and is presently not fully
understood. Human B cells in mononuclear cell preparations but not
purified Beta cells incubated with recombinant IL-4 (riL-4) secrets
IgE/IgG4, suggesting that a non-B cell population is necessary for human
rIL-4 induced IgE secretion. In addition, we found that polyclonal Beta
cell activators inhibit the human rIL-4 induced IgE/IgG4 secretion.
Another unresolved issue in Il-4 induced IgE formation is the
preferential interaction of allergens with IL-4 producing T helper cells.
Preliminary experiments in mice suggest that antigen presenting cells may
play an important role in causing T helper cells to differentiate into
IL-4 secreting cells.

The goal of the proposed research is centered on three open questions
regarding IL-4 induced IgE secretion: 1) What are the cellular
requirements for human rIL-4 induced IgE/IgG4 secretion in vitro? What is
the role of antigen-presenting cells in the differentiation of T helper
cells to become IL-4 secreting cells? 3) Do human allergen specific T
cell clones secrete IL-4 but not IL-2/IFN-gamma?

The specific aims are:  1) to study the cellular requirement for human
rIL-4 induced IgE/IgG4 secretion in vitro and to characterize the Beta
cells responding to rIL-4.  2) To analyze the mechanism of suppression of
rIL-4 induced IgE/IgG4 secretion by Beta cell activators.  3) To
determine whether dendritic cells obtained from different anatomic
locations cause differentiation of PHA-responsive murine T cell clones
into either IL-4 or IFN-gamma secreting cells.  4) To quantitate the IL-
4, IL-2 and IFN-gamma production by allergen-specific human T cell clones
and to use allergen specific T cell clones to develop a human polyclonal
Beta cell activation system by coupling the allergen to purified anti-
human IgM.

## Key facts

- **NIH application ID:** 3124800
- **Project number:** 7R01AI010734-17
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **SAM.gov UEI:** UYTTZT6G9DT1
- **Principal Investigator:** HANS L SPIEGELBERG
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $184,519
- **Award type:** 7
- **Project period:** 1990-08-01 → 1992-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124800

## Citation

> US National Institutes of Health, RePORTER application 3124800, IGE AND IGG SUBCLASS FORMATION (7R01AI010734-17). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124800. Licensed CC0.

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