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The monoclonal antibody HB1 recognizes an adhesion molecule for macrophages in the brain
1Oxford University, Department of Pharmacology, UK.
Abstract:
The brain environment exerts a powerful influence on macrophage phenotype, as exemplified by microglia, but the mechanisms mediating this control are nuclear. Since adhesion molecules are known to transmit signals across cell membranes, we investigated adhesion receptors involved in macrophage interaction with brain tissue. We have demonstrated previously that macrophages adhere specifically to CNS neurones in an in vitro assay. Here we show that this adhesion is inhibited by lectins, including Griffonia simplicofolia isolectin B4 (GSI), which has been used as a microglial marker for many years. Adhesion is unaffected by antibodies to several known adhesion molecules but is markedly inhibited by a new monoclonal antibody: HB1. HB1 recognizes microglia in the normal brain and activated microglia and recruited monocytes during CNS pathology. It labels a subset of resident macrophages and recruited monocytes in other tissues. Using this antibody, we isolated a protein of about 110 kDa from macrophage cell lysates. This protein is recognized by GSI, providing the first evidence of a functional role for the antigen labelled by this lectin. Further study of the HB1 antigen may provide important information about the influence of the brain environment on the phenotype of monocytic cells.
Insights
Researchers identified a novel protein, the HB1 antigen, crucial for macrophage adhesion to neurons. This discovery sheds light on how the brain environment influences immune cell behavior, particularly microglia.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- The brain microenvironment significantly shapes macrophage phenotypes, notably microglia.
- Adhesion molecules are key mediators of intercellular signaling and cell-cell interactions.
Purpose of the Study:
- To investigate adhesion receptors mediating macrophage interaction with central nervous system (CNS) neurons.
- To identify the molecular mechanisms underlying specific macrophage-neuron adhesion.
Main Methods:
- Utilized an in vitro assay to study macrophage adhesion to CNS neurons.
- Employed lectins like Griffonia simplicofolia isolectin B4 (GSI) and a novel monoclonal antibody (HB1) to probe adhesion mechanisms.
- Isolated and characterized a protein recognized by the HB1 antibody and GSI.
Main Results:
- Macrophage adhesion to CNS neurons was specifically inhibited by GSI and markedly by the HB1 antibody.
- The HB1 antibody identified microglia in normal and pathological CNS conditions, as well as monocytes in other tissues.
- A ~110 kDa protein, recognized by GSI, was isolated using the HB1 antibody, suggesting a functional role for the GSI-labeled antigen.
Conclusions:
- The HB1 antigen is involved in macrophage-neuronal adhesion and is recognized by GSI.
- This study provides the first evidence for a functional role of the GSI-labeled antigen in macrophage-brain interactions.
- Further investigation of the HB1 antigen may elucidate how the brain environment influences monocytic cell phenotypes.