# DEPLETION OF FC RECEPTORS DURING IMMUNE CLEARANCE

> **NIH NIH R01** · DUKE UNIVERSITY · 1987 · $145,601

## Abstract

Small amounts of a monoclonal IgG anti-Fc receptor antibody (2.4G2 prepared
by Dr. J. Unkeless of the Rockefeller Institute) or other anti-leukocyte
antibodies and tenfold greater amounts of IgG aggregates, potently block Fc
receptor function and to a lesser extent also block other MPS function in
normal mice in vivo.  Since monoclonal antibodies might be useful
therapeutic agents for treating such autoimmune blood distruction in vivo,
and IgG aggregates share many functional traits with clinically significant
immune complexes, the following studies propose:  1.) to characterize the
effects of 2.4G2, Fab2 fragments of 2.4G2, anti-leukocyte antibodies and
IgG aggregates (or immune complexes) on MPS function.  To this end, the
clearance of IgG coated red cells and of several other radiolabeled ligands
which are cleared by other mechanisms by mononuclear phagocytes,
endothelial cells or liver parenchymal cells will be assessed.  The
mechanism by which monoclonal antibodies or IgG complexes suppress Fc
receptor mediated, and other types of MPS clearance will be assessed by
studying their effects on mononuclear cell phagocytic function and serum
opsonic activity in vitro.  2.) to assess the efficacy and safety of 2.4G2
(and other blockers of MPS function), the effects of these agents on the
rate of red cell turnover, on the level of red cell antibody, and on the
level of circulating immune complexes will be assessed in normal and
auto-immune mice, induced to develop autoimmune hemolysis by the infusion
of rat red cells; and in NZB mice which develop autoimmune hemolysis
spontaneously.  3.) to assess the importance of Fc receptor function and
other aspects of MPS function in immune complex disease, the effect of
2.4G2 and other blockers on the clinical severity of autoimmune disease, on
the levels of circulating immune complexes and on the degree of complex
deposition in the kidney will be assessed in autoimmune animals.  4.) To
better understand the spontaneous MPS defects observed in asymptomatic and
symptomatic mice of strains susceptible to autoimmune disease, these
defects will be characterized as in 1.).  If these defects resemble those
produced by anti-leukocyte antibodies and circulating immune complexes,
attempts will be made to demonstrate humoral transmission of defects in
vitro and in vivo.  Since these studies are concerned with the physiologic
effects of both monoclonal antibodies and immune complexes in vivo, they
may have value both for those evaluating the therapeutic value of
monoclonal antibodies, and for studying the pathophysiology of autoimmune
disease.

## Key facts

- **NIH application ID:** 3127660
- **Project number:** 5R01AI018073-07
- **Recipient organization:** DUKE UNIVERSITY
- **SAM.gov UEI:** TP7EK8DZV6N5
- **Principal Investigator:** ROGER J KURLANDER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $145,601
- **Award type:** 5
- **Project period:** 1981-08-01 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127660

## Citation

> US National Institutes of Health, RePORTER application 3127660, DEPLETION OF FC RECEPTORS DURING IMMUNE CLEARANCE (5R01AI018073-07). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3127660. Licensed CC0.

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