Title
Experimental African trypanosome infection by needle passage or natural tsetse fly challenge thwarts the development of collagen-induced arthritis in DBA/1 prone mice via an impairment of antigen specific B cell autoantibody titers Experimental African trypanosome infection by needle passage or natural tsetse fly challenge thwarts the development of collagen-induced arthritis in DBA/1 prone mice via an impairment of antigen specific B cell autoantibody titers
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
Publication type
article
Publication
Subject
Engineering sciences. Technology
Source (journal)
PLoS ONE
Volume/pages
10(2015) :6 , 10 p.
ISSN
1932-6203
1932-6203
Article Reference
e0130431
Carrier
E-only publicatie
Target language
English (eng)
Full text (Publishers DOI)
Abstract
Collagen-induced arthritis is a B cell-mediated autoimmune disease. Recently published studies have demonstrated that in some rare cases pathogens can confer protection from autoimmunity. Trypanosoma brucei parasites are tsetse fly transmitted extracellular protozoans causing sleeping sickness disease in humans and Nagana in livestock in sub-Saharan endemic areas. In the past, we demonstrated that trypanosome infections impair B cell homeostasis and abolish vaccine-induced protection against unrelated antigens. Hence, here we hypothesized that trypanosome infection can affect the onset of CIA by specifically dampening specific B-cell responses and type II collagen antibody titers in DBA/1 prone mice. We observed a substantial delay in the onset of collagen-induced arthritis in T. brucei-infected DBA/1mice that correlates with a drastic decrease of type II collagen titers of the different IgG isotypes in the serum. Treatment of infected mice with Berenil, a trypanocidal drug, restored the development of CIA-associated clinical symptoms. Interestingly, these data were confirmed by the challenge of immunized DBA/1 prone mice with T. brucei-infected tsetse flies. Together, these results demonstrate that T. brucei infection is impairing the maintenance of the antigen specific plasma B cell pool driving the development of CIA in DBA/1 prone mice.
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Full text (open access)
https://repository.uantwerpen.be/docman/irua/9ba536/130109.pdf
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