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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
Optimization of Folate-Targeted Immunotherapy for the Treatment of Experimental Arthritis
Bindu Varghese1, Chrystal Paulos1, Philip S Low2
1Department of Chemistry, Purdue University, 720 Clinic Drive, West Lafayette, IN, 47907-2084, USA.
Folate-targeted immunotherapy constitutes a powerful method for the treatment of established arthritis in multiple animal models of the disease. The therapy involves immunization of the animal against a hapten to induce anti-hapten antibodies, followed by injection with a folate-hapten conjugate to decorate the surface of folate receptor-positive (activated) macrophages with the antigenic hapten. The hapten-marked macrophages are then recognized by the anti-hapten antibodies and eliminated by immune mechanisms, leading to attenuation of disease symptoms. In the following paper, we optimize the therapy for elimination of inflammatory macrophages and suppression of rheumatoid arthritis symptoms. We also demonstrate a tight correlation between folate receptor-positive macrophage abundance in the liver and inflammation of affected joints. The results suggest that therapies that reduce folate receptor-positive macrophage populations in the body should constitute effective treatments for rheumatoid arthritis.
Folate-targeted immunotherapy constitutes a powerful method for the treatment of established arthritis in multiple animal models of the disease. The therapy involves immunization of the animal against a hapten to induce anti-hapten antibodies, followed by injection with a folate-hapten conjugate to decorate the surface of folate receptor-positive (activated) macrophages with the antigenic hapten. The hapten-marked macrophages are then recognized by the anti-hapten antibodies and eliminated by immune mechanisms, leading to attenuation of disease symptoms. In the following paper, we optimize the therapy for elimination of inflammatory macrophages and suppression of rheumatoid arthritis symptoms. We also demonstrate a tight correlation between folate receptor-positive macrophage abundance in the liver and inflammation of affected joints. The results suggest that therapies that reduce folate receptor-positive macrophage populations in the body should constitute effective treatments for rheumatoid arthritis.
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