The IgG specific endoglycosidase EndoS inhibits both cellular and complement mediated autoimmune hemolysis.
Allhorn, Maria LU ; Briceño, Juana G ; Baudino, Lucie ; Lood, Christian LU ; Olsson, Martin L LU
; Izui, Shozo
and Collin, Mattias
LU
(2010)
In Blood
115(24).
p.5080-5088
- Abstract
- EndoS from Streptococcus pyogenes is an immunomodulating enzyme that specifically hydrolyzes glycans from human IgG and thereby affects antibody effector functions. Autoimmune hemolytic anemia is caused by antibody mediated red blood cell (RBC) destruction and often resists treatment with corticosteroids that also cause frequent adverse effects. We show here that anti-RhD (anti-D) and rabbit anti-human-RBC antibodies (anti-RBC) mediated destruction of RBC, i.e. phagocytosis, complement activation and hemolysis in vitro and in vivo was inhibited by EndoS. Phagocytosis by monocytes in vitro was inhibited by pre-treatment of anti-D with EndoS before sensitization of RBC, and abrogated by direct addition of EndoS to blood containing sensitized... (More)
- EndoS from Streptococcus pyogenes is an immunomodulating enzyme that specifically hydrolyzes glycans from human IgG and thereby affects antibody effector functions. Autoimmune hemolytic anemia is caused by antibody mediated red blood cell (RBC) destruction and often resists treatment with corticosteroids that also cause frequent adverse effects. We show here that anti-RhD (anti-D) and rabbit anti-human-RBC antibodies (anti-RBC) mediated destruction of RBC, i.e. phagocytosis, complement activation and hemolysis in vitro and in vivo was inhibited by EndoS. Phagocytosis by monocytes in vitro was inhibited by pre-treatment of anti-D with EndoS before sensitization of RBC, and abrogated by direct addition of EndoS to blood containing sensitized RBC. The toxic effects of monocytes stimulated with anti-D-sensitized RBC, as measured by interleukin-8 secretion and oxygen metabolite production, was restrained by EndoS. Agglutination of RBC and complement mediated hemolysis in vitro in whole human blood caused by rabbit anti-RBC was inhibited by EndoS. Development of anemia in mice caused by a murine anti-RBC IgG2a monoclonal autoantibody, and complement activation and erythrophagocytosis by Kupffer cells in the liver, were reduced by EndoS. Our data indicate that EndoS is a potential therapeutic agent that might be evaluated as an alternative to current treatment regimens against antibody mediated destruction of RBC. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1598705
- author
- Allhorn, Maria
LU
; Briceño, Juana G
; Baudino, Lucie
; Lood, Christian
LU
; Olsson, Martin L
LU
; Izui, Shozo
and Collin, Mattias
LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- 115
- issue
- 24
- pages
- 5080 - 5088
- publisher
- American Society of Hematology
- external identifiers
-
- wos:000278888900018
- pmid:20357243
- scopus:77954680167
- pmid:20357243
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2009-08-239020
- language
- English
- LU publication?
- yes
- id
- 77726d1d-536a-4288-a057-e0ebdbdcafe6 (old id 1598705)
- alternative location
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890147/
- date added to LUP
- 2016-04-01 09:57:50
- date last changed
- 2022-04-04 01:05:19
@article{77726d1d-536a-4288-a057-e0ebdbdcafe6,
abstract = {{EndoS from Streptococcus pyogenes is an immunomodulating enzyme that specifically hydrolyzes glycans from human IgG and thereby affects antibody effector functions. Autoimmune hemolytic anemia is caused by antibody mediated red blood cell (RBC) destruction and often resists treatment with corticosteroids that also cause frequent adverse effects. We show here that anti-RhD (anti-D) and rabbit anti-human-RBC antibodies (anti-RBC) mediated destruction of RBC, i.e. phagocytosis, complement activation and hemolysis in vitro and in vivo was inhibited by EndoS. Phagocytosis by monocytes in vitro was inhibited by pre-treatment of anti-D with EndoS before sensitization of RBC, and abrogated by direct addition of EndoS to blood containing sensitized RBC. The toxic effects of monocytes stimulated with anti-D-sensitized RBC, as measured by interleukin-8 secretion and oxygen metabolite production, was restrained by EndoS. Agglutination of RBC and complement mediated hemolysis in vitro in whole human blood caused by rabbit anti-RBC was inhibited by EndoS. Development of anemia in mice caused by a murine anti-RBC IgG2a monoclonal autoantibody, and complement activation and erythrophagocytosis by Kupffer cells in the liver, were reduced by EndoS. Our data indicate that EndoS is a potential therapeutic agent that might be evaluated as an alternative to current treatment regimens against antibody mediated destruction of RBC.}},
author = {{Allhorn, Maria and Briceño, Juana G and Baudino, Lucie and Lood, Christian and Olsson, Martin L and Izui, Shozo and Collin, Mattias}},
issn = {{1528-0020}},
language = {{eng}},
number = {{24}},
pages = {{5080--5088}},
publisher = {{American Society of Hematology}},
series = {{Blood}},
title = {{The IgG specific endoglycosidase EndoS inhibits both cellular and complement mediated autoimmune hemolysis.}},
url = {{http://dx.doi.org/10.1182/blood-2009-08-239020}},
doi = {{10.1182/blood-2009-08-239020}},
volume = {{115}},
year = {{2010}},
}