Treating murine inflammatory diseases with an anti-erythrocyte antibody
| Autor: | Danielle Marjoram, Alan H. Lazarus, Ian K. Campbell, Michael Kim, Patrick J. Mott, Jennifer Brasseit, Chao Ching Jen, Andrew R. Crow, Rick Kapur, Simrat S Kahlon, Adrian Zuercher, Yoelys Cruz-Leal, Sandra Koernig, Issaka Yougbaré, Fabian Käsermann, Ramsha Khan, Alaa Amash, Heyu Ni, John W. Semple |
|---|---|
| Přispěvatelé: | Landsteiner Laboratory |
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Chemokine Erythrocytes Glycosylation Acute Lung Injury Arthritis Mice SCID Lung injury Monocytes 03 medical and health sciences 0302 clinical medicine Immune system Cell Movement Animals Medicine CXCL10 Blood Transfusion Inflammation Purpura Thrombocytopenic Idiopathic biology business.industry Monocyte Receptors IgG Antibodies Monoclonal Anemia General Medicine medicine.disease Arthritis Experimental Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure Immunoglobulin G Immunology Disease Progression biology.protein CXCL9 Chemokines Inflammation Mediators Antibody business 030215 immunology |
| Zdroj: | Science translational medicine, 11(506):eaau8217. American Association for the Advancement of Science |
| ISSN: | 1946-6234 |
| Popis: | Treatment of autoimmune and inflammatory diseases typically involves immune suppression. In an opposite strategy, we show that administration of the highly inflammatory erythrocyte-specific antibody Ter119 into mice remodels the monocyte cellular landscape, leading to resolution of inflammatory disease. Ter119 with intact Fc function was unexpectedly therapeutic in the K/BxN serum transfer model of arthritis. Similarly, it rapidly reversed clinical disease progression in collagen antibody-induced arthritis (CAIA) and collagen-induced arthritis and completely corrected CAIA-induced increase in monocyte Fcγ receptor II/III expression. Ter119 dose-dependently induced plasma chemokines CCL2, CCL5, CXCL9, CXCL10, and CCL11 with corresponding alterations in monocyte percentages in the blood and liver within 24 hours. Ter119 attenuated chemokine production from the synovial fluid and prevented the accumulation of inflammatory cells and complement components in the synovium. Ter119 could also accelerate the resolution of hypothermia and pulmonary edema in an acute lung injury model. We conclude that this inflammatory anti-erythrocyte antibody simultaneously triggers a highly efficient anti-inflammatory effect with broad therapeutic potential. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|