# IMMUNOREGULATION OF MURINE MYELOMA

> **NIH NIH R01** · UNIVERSITY OF IOWA · 1988 · $152,965

## Abstract

This is a proposal to continue our studies on the immunological mechanisms
that regulate the growth and immunoglobulin expression in murine
plasmacytoma cells.  A major objective is to extend our previous findings
on the molecular mechanisms by which suppressor T cells specific for the
idiotypic antigens expressed on the IgA lambda2 TNP-specific protein (M315)
inhibit the synthesis and secretion of M315 by the BALB/c plasmacytoma
MOPC-315.  Suppression of M315 synthesis is triggered by a VH315-specific
suppressor T cell induced by immunization of BALB/c mice with M315 or
VH315.  This suppressor cell produces a product that inhibits the
expression of lambda2 mRNA in MOPC-315 cells without influencing the
expression of alpha mRNA or J chain mRNA, and without influencing the
synthesis of other proteins in MOPC-315 cells.  Suppression of lambda2 mRNA
is accompanied by the coordinate suppression of the trans located
aberrantly rearranged lambda1 gene in MOPC-315 cells.  Experiments are
designed to determine if the trans regulation:  a) is at the level of
transcription, and b) involves activation of an endogenous repressor of
light chain gene expression.  MOPC-315 hybridomas that express a second
monoclonal immunoglobulin, and MOPC-315 cells that express light chain
genes introduced by transfection will be used to establish whether the
light chain regulation is specific for lambda or lambda plus kappa light
chains.  Comparable studies will be carried out to investigate the
mechanism of suppression of M460 synthesis in the IgA kappa, TNP-specific
MOPC-460 plasmacytoma.  Experiments will be done to determine if
suppression and enhancement of M315 secretion by TNP-antigen specific
regulation also involves the control of light chain expression.  A third
major objective is to further investigate the mechanisms that mediate
idiotype-specific tumor immunity against plasmacytoma cells.

These studies will develop important new information about the basic
mechanisms by which immunoregulatory T cells control immunoglobulin
expression in B cells and may provide the basic knowledge necessary to
develop idiotype-specific regulatory strategies for the control of
malignant B cells in humans.

## Key facts

- **NIH application ID:** 3170262
- **Project number:** 5R01CA032275-08
- **Recipient organization:** UNIVERSITY OF IOWA
- **SAM.gov UEI:** Z1H9VJS8NG16
- **Principal Investigator:** RICHARD G. LYNCH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $152,965
- **Award type:** 5
- **Project period:** 1981-07-01 → 1989-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3170262

## Citation

> US National Institutes of Health, RePORTER application 3170262, IMMUNOREGULATION OF MURINE MYELOMA (5R01CA032275-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3170262. Licensed CC0.

---

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