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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Folate receptor-β constitutes a marker for human proinflammatory monocytes.

Jiayin Shen¹, Andrew R Hilgenbrink¹, Wei Xia¹

¹Department of Chemistry, Purdue University, West Lafayette, Indiana, USA;

Journal of Leukocyte Biology

|July 13, 2014

Summary

This summary is machine-generated.

Folates receptor beta (FR-β) is uniquely expressed on pro-inflammatory monocytes. This finding offers a new strategy to target and suppress the migration of these inflammatory monocytes in autoimmune diseases.

Keywords:

folate targeting immunotherapy inflammation inflammatory subset

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Area of Science:

Immunology
Cell Biology
Rheumatology

Background:

Activated macrophages play a key role in inflammatory and autoimmune diseases.
Macrophages are known to overexpress Folate Receptor beta (FR-β).
FR-targeted therapies show promise for inflammatory diseases, but expression on other cells is unclear.

Purpose of the Study:

To investigate the expression of FR-β on various hematopoietic cells.
To identify specific monocyte subsets expressing FR-β.
To explore FR-β as a potential therapeutic target for autoimmune diseases.

Main Methods:

Analysis of peripheral blood cells using a monoclonal antibody (mAb) to human FR-β.
Molecular characterization of FR-β expressing monocytes.
Assessment of folate-binding capacity and co-expression of inflammatory markers (CCR2, HLA-DR).
Analysis of synovial monocytes from Rheumatoid Arthritis (RA) patients.

Main Results:

Only monocytes, specifically the classic/pro-inflammatory subset (CD14(high)CD16(-)), express FR-β.
FR-β positive monocytes exhibit folate-binding capabilities.
FR-β co-expresses with pro-inflammatory markers CCR2 and HLA-DR on monocytes.
Synovial monocytes from RA patients also express FR-β.

Conclusions:

FR-β is uniquely expressed on the pro-inflammatory monocyte subset.
This specific expression pattern provides a novel target for therapeutic strategies.
Targeting FR-β may suppress the migration of inflammatory monocytes into inflamed tissues, aiding autoimmune disease treatment.