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Treating murine inflammatory diseases with an anti-erythrocyte antibody

Crow, Andrew R. ; Kapur, Rick LU ; Koernig, Sandra ; Campbell, Ian K. ; Jen, Chao Ching ; Mott, Patrick J. ; Marjoram, Danielle ; Khan, Ramsha ; Kim, Michael and Brasseit, Jennifer , et al. (2019) In Science Translational Medicine 11(506).
Abstract

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... (More)

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.

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publication status
published
subject
in
Science Translational Medicine
volume
11
issue
506
article number
eaau8217
publisher
American Association for the Advancement of Science (AAAS)
external identifiers
  • pmid:31434758
  • scopus:85071306729
ISSN
1946-6234
DOI
10.1126/scitranslmed.aau8217
language
English
LU publication?
yes
id
b08e5aba-7380-47c4-a7d5-e1edda03db56
date added to LUP
2019-12-03 10:13:42
date last changed
2020-04-07 05:40:29
@article{b08e5aba-7380-47c4-a7d5-e1edda03db56,
  abstract     = {<p>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.</p>},
  author       = {Crow, Andrew R. and Kapur, Rick and Koernig, Sandra and Campbell, Ian K. and Jen, Chao Ching and Mott, Patrick J. and Marjoram, Danielle and Khan, Ramsha and Kim, Michael and Brasseit, Jennifer and Cruz-Leal, Yoelys and Amash, Alaa and Kahlon, Simrat and Yougbare, Issaka and Ni, Heyu and Zuercher, Adrian W. and Käsermann, Fabian and Semple, John W. and Lazarus, Alan H.},
  issn         = {1946-6234},
  language     = {eng},
  month        = {08},
  number       = {506},
  publisher    = {American Association for the Advancement of Science (AAAS)},
  series       = {Science Translational Medicine},
  title        = {Treating murine inflammatory diseases with an anti-erythrocyte antibody},
  url          = {http://dx.doi.org/10.1126/scitranslmed.aau8217},
  doi          = {10.1126/scitranslmed.aau8217},
  volume       = {11},
  year         = {2019},
}