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PMID: 8547680 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Monoclonal antibody 7G3 recognizes the N-terminal domain of the human interleukin-3 (IL-3) receptor alpha-chain and functions as a specific IL-3 receptor antagonist.

Blood ·Vol. 87 ·No. 1 ·1996-01-01 ·Pages 83-92

Sun Q, Woodcock JM, Rapoport A, Stomski FC, Korpelainen EI, Bagley CJ, Goodall GJ, Smith WB, Gamble JR, Vadas MA, Lopez AF

Abstract

The human interleukin-3 receptor (IL-3R) is expressed on myeloid, lymphoid, and vascular endothelial cells, where it transduces IL-3-dependent signals leading to cell activation. Although IL-3R activation may play a role in hematopoiesis and immunity, its aberrant expression or excessive stimulation may contribute to pathologic conditions such as leukemia, lymphoma, and allergic reactions. We describe here the generation and characterization of a monoclonal antibody (MoAb), 7G3, which specifically binds to the IL-3R alpha-chain and completely abolishes its function. MoAb 7G3 immunoprecipitated and recognized in Western blots the IL-3R alpha-chain expressed by transfected cells and bound to primary cells expressing IL-3R alpha. MoAb 7G3 bound the IL-3R alpha-chain with a kd of 900 pmol/L and inhibited 125I-IL-3 binding to high- and low-affinity receptors in a dose-dependent manner. Conversely, IL-3 but not granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibited 125I-7G3 binding to high- and low-affinity IL-3Rs, indicating that MoAb 7G3 and IL-3 bind to common or adjacent sites. In keeping with the inhibition of IL-3 binding, MoAb 7G3 antagonized IL-3 biologic activities, namely stimulation of TF-1 cell proliferation, basophil histamine release, and IL-6 and IL-8 secretion from human endothelial cells. Two other anti-IL-3R alpha-chain MoAbs failed to inhibit IL-3 binding or function. Epitope mapping experiments using truncated IL-3R alpha-chain mutants and IL-3R alpha/GM-CSFR alpha chimeras revealed that 31 amino acids in the N-terminus of IL-3R alpha were required for MoAb 7G3 binding. MoAb 7G3 may be of clinical significance for antagonizing IL-3 in pathologic conditions such as some myeloid leukemias, follicular B-cell lymphoma, and allergy. Furthermore, these results implicate the N-terminal domain of IL-3R alpha in IL-3 binding. Since this domain is unique to the IL-3/GM-CSF/IL-5 receptor subfamily, it may represent a novel and common binding feature in these receptors.

MeSH Terms
Animals Antibodies, Monoclonal/immunology,pharmacology Antibody Specificity Basophils/drug effects,metabolism Binding, Competitive CHO Cells Cell Division/drug effects Cell Line Cricetinae Cricetulus Endothelium, Vascular/drug effects Histamine Release/drug effects Humans Interleukin-3/metabolism,pharmacology Mice Mice, Inbred BALB C Receptors, Interleukin-3/antagonists & inhibitors,chemistry,immunology Recombinant Fusion Proteins/antagonists & inhibitors,chemistry
Chemicals
Antibodies, Monoclonal Interleukin-3 Receptors, Interleukin-3 Recombinant Fusion Proteins
Authors & Affiliations
11 authors, click to expand affiliations / ORCID
Sun Q
Division of Human Immunology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Adelaide, South Australia.
Woodcock J M
Rapoport A
Stomski F C
Korpelainen E I
Bagley C J
Goodall G J
Smith W B
Gamble J R
Vadas M A
Lopez A F
Article Info
Journal
Blood
Abbr.
Blood
ISSN
0006-4971
Published
1996-01-01
Pages
83-92
Language
English
Region
United States
NLM ID
7603509
Subset
IM
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