Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.

Anemia caused by trypanosome infection is poorly understood. Autoimmunity during Trypanosoma brucei infection was proposed to have a role during anemia, but the mechanisms involved during this pathology have not been elucidated. In mouse models and human patients infected with malaria parasites, aty...

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Autores principales: Juan Rivera-Correa, Joseph Verdi, Julian Sherman, Jeremy M Sternberg, Jayne Raper, Ana Rodriguez
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Publicado: Public Library of Science (PLoS) 2021
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Acceso en línea:https://doaj.org/article/75eca697b21141c1ba78895455e9cb51
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spelling oai:doaj.org-article:75eca697b21141c1ba78895455e9cb512021-12-02T20:24:01ZAutoimmunity to phosphatidylserine and anemia in African Trypanosome infections.1935-27271935-273510.1371/journal.pntd.0009814https://doaj.org/article/75eca697b21141c1ba78895455e9cb512021-09-01T00:00:00Zhttps://doi.org/10.1371/journal.pntd.0009814https://doaj.org/toc/1935-2727https://doaj.org/toc/1935-2735Anemia caused by trypanosome infection is poorly understood. Autoimmunity during Trypanosoma brucei infection was proposed to have a role during anemia, but the mechanisms involved during this pathology have not been elucidated. In mouse models and human patients infected with malaria parasites, atypical B-cells promote anemia through the secretion of autoimmune anti-phosphatidylserine (anti-PS) antibodies that bind to uninfected erythrocytes and facilitate their clearance. Using mouse models of two trypanosome infections, Trypanosoma brucei and Trypanosoma cruzi, we assessed levels of autoantibodies and anemia. Our results indicate that acute T. brucei infection, but not T. cruzi, leads to early increased levels of plasma autoantibodies against different auto antigens tested (PS, DNA and erythrocyte lysate) and expansion of atypical B cells (ABCs) that secrete these autoantibodies. In vitro studies confirmed that a lysate of T. brucei, but not T. cruzi, could directly promote the expansion of these ABCs. PS exposure on erythrocyte plasma membrane seems to be an important contributor to anemia by delaying erythrocyte recovery since treatment with an agent that prevents binding to it (Annexin V) ameliorated anemia in T. brucei-infected mice. Analysis of the plasma of patients with human African trypanosomiasis (HAT) revealed high levels of anti-PS antibodies that correlated with anemia. Altogether these results suggest a relation between autoimmunity against PS and anemia in both mice and patients infected with T. brucei.Juan Rivera-CorreaJoseph VerdiJulian ShermanJeremy M SternbergJayne RaperAna RodriguezPublic Library of Science (PLoS)articleArctic medicine. Tropical medicineRC955-962Public aspects of medicineRA1-1270ENPLoS Neglected Tropical Diseases, Vol 15, Iss 9, p e0009814 (2021)
institution DOAJ
collection DOAJ
language EN
topic Arctic medicine. Tropical medicine
RC955-962
Public aspects of medicine
RA1-1270
spellingShingle Arctic medicine. Tropical medicine
RC955-962
Public aspects of medicine
RA1-1270
Juan Rivera-Correa
Joseph Verdi
Julian Sherman
Jeremy M Sternberg
Jayne Raper
Ana Rodriguez
Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
description Anemia caused by trypanosome infection is poorly understood. Autoimmunity during Trypanosoma brucei infection was proposed to have a role during anemia, but the mechanisms involved during this pathology have not been elucidated. In mouse models and human patients infected with malaria parasites, atypical B-cells promote anemia through the secretion of autoimmune anti-phosphatidylserine (anti-PS) antibodies that bind to uninfected erythrocytes and facilitate their clearance. Using mouse models of two trypanosome infections, Trypanosoma brucei and Trypanosoma cruzi, we assessed levels of autoantibodies and anemia. Our results indicate that acute T. brucei infection, but not T. cruzi, leads to early increased levels of plasma autoantibodies against different auto antigens tested (PS, DNA and erythrocyte lysate) and expansion of atypical B cells (ABCs) that secrete these autoantibodies. In vitro studies confirmed that a lysate of T. brucei, but not T. cruzi, could directly promote the expansion of these ABCs. PS exposure on erythrocyte plasma membrane seems to be an important contributor to anemia by delaying erythrocyte recovery since treatment with an agent that prevents binding to it (Annexin V) ameliorated anemia in T. brucei-infected mice. Analysis of the plasma of patients with human African trypanosomiasis (HAT) revealed high levels of anti-PS antibodies that correlated with anemia. Altogether these results suggest a relation between autoimmunity against PS and anemia in both mice and patients infected with T. brucei.
format article
author Juan Rivera-Correa
Joseph Verdi
Julian Sherman
Jeremy M Sternberg
Jayne Raper
Ana Rodriguez
author_facet Juan Rivera-Correa
Joseph Verdi
Julian Sherman
Jeremy M Sternberg
Jayne Raper
Ana Rodriguez
author_sort Juan Rivera-Correa
title Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
title_short Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
title_full Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
title_fullStr Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
title_full_unstemmed Autoimmunity to phosphatidylserine and anemia in African Trypanosome infections.
title_sort autoimmunity to phosphatidylserine and anemia in african trypanosome infections.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/75eca697b21141c1ba78895455e9cb51
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AT josephverdi autoimmunitytophosphatidylserineandanemiainafricantrypanosomeinfections
AT juliansherman autoimmunitytophosphatidylserineandanemiainafricantrypanosomeinfections
AT jeremymsternberg autoimmunitytophosphatidylserineandanemiainafricantrypanosomeinfections
AT jayneraper autoimmunitytophosphatidylserineandanemiainafricantrypanosomeinfections
AT anarodriguez autoimmunitytophosphatidylserineandanemiainafricantrypanosomeinfections
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