# REGULATION OF IMMUNOGLOBULIN CLASS EXPRESSION

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 1989 · $95,596

## Abstract

The purpose of this proposal is to determine how the different
antibody classes or isotypes are regulated with emphasis on the
role of the helper T cell.  The majority of foreign antigens give
rise to an antibody response diverse in isotypes.  Therefore, it
has been difficult to determine how isotypes can be individually
regulated.  However, some infectious organisms result in the
production of one or two isotypes such as the parasite
Mesocestoides corti which results in a dramatic increase in IgG1
with little or no effect on the other non-IgM isotypes.  Using this
physiological model systems, the control of IgG1 production will
be studied at both cellular and molecular levels.  Helper T cells
clones derived from parasite infected animals appear to both
enhance IgG1 and downregulate the remaining isotypes in vitro.
Using cloned populations of cells and B cell limit dilution assays
the mechanism of restriction to IgM and IgG1 will be delineated
by determining the B cell target, the role of T cell derived
soluble mediators, and the way in which the live parasite
stimulates regulatory T cells.  In this way, the mode of action of
isotype restricting T cell clones will be determining which may
involve mechanisms of induction, selection, and/or some type of
suppression.  In addition, the molecular mechanism of isotype
restriction will be analyzed using a combination of in situ
hybridization of single cells, Northern blot hybridizations, and
Southern blot hybridization with several heavy chain specific
probes.  Moreover, the necessity for isotype switch
recombination for IgG1 expression will be tested.  These studies
should contribute substantially to our overall understanding of
antibody class expression as well as elucidate mechanism by
which isotypes can be individually regulated.  This is essential so
that certain isotypes can be manipulated in disease states such
as the IgE isotype which cause allergy.

## Key facts

- **NIH application ID:** 3129875
- **Project number:** 5R01AI020313-06
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **SAM.gov UEI:** C3KXNLTAAY98
- **Principal Investigator:** JUDY M TEALE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $95,596
- **Award type:** 5
- **Project period:** 1984-09-01 → 1992-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3129875

## Citation

> US National Institutes of Health, RePORTER application 3129875, REGULATION OF IMMUNOGLOBULIN CLASS EXPRESSION (5R01AI020313-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3129875. Licensed CC0.

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