IDIOTYPE-ANTI-IDIOTYPE MODULATION OF IMMUNITY TO M-MULV

NIH RePORTER · NIH · R01 · $178,640 · view on reporter.nih.gov ↗

Abstract

Tumors and infectious diseases are among the more important problems facing surgeons. This proposal is designed to evaluate mechanisms by which monoclonal antibodies may modulate host defense against retrovirus induced tumors and may have implications for other surgically important problems such as pre- and post operative infection, transplantation and other retrovisus induced diseases. Two major approaches are taken (1) monoclonal antibodies may function immunotherapeutically and (2) idiotype regulation can be a major factor to Ii influence immunity to tumors and/or infection. We propose that (1) monoclonal antibodies (AB1) with specificity for retrovirus induced tumor antigens can effectively inhibit tumor growth, (2) they can induce anti-idiotypic (Ab2) and anti-anti-idiotypic (Ab3) responses a component of which (Ab1) binds antigen, and (3) further that monoclonal anti-idiotypic antibody (Ab2) can be used as a vaccine in the absence of antigen to preimmunize against tumor growth, but (4) may induce tumor enhancement if administered following tumor induction, and (5) that Ab1 or Ab2 may alter immunologic memory. The experiments proposed to test this hypothesis will be conducted with the Moloney leukemia virus (M-MuLV) and Moloney Sarcoma virus (M-MuSV) induced tumors in BALB/c mice. Our previous experiments have indicated a promising feasibility of these studies which may have relevance to other surgically important diseases in addition to tumors.

Key facts

NIH application ID
3175991
Project number
2R01CA038008-04
Recipient
UNIVERSITY OF ALABAMA AT BIRMINGHAM
SAM.gov UEI
YND4PLMC9AN7
Principal Investigator
EDDIE W LAMON
Activity code
R01
Funding institute
NIH
Fiscal year
1990
Award amount
$178,640
Award type
2
Project period
1987-08-19 → 1993-07-31