Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice
Autor(a) principal: | |
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Data de Publicação: | 2006 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Memórias do Instituto Oswaldo Cruz |
Texto Completo: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762006000500007 |
Resumo: | Immune responses to malaria infections are characterized by strong T and B cell activation, which, in addition of potentially causing immunopathology, are of poor efficacy against the infection. It is possible that the thymus is involved in the origin of immunopathological reactions and a target during malaria infections. This work was developed in an attempt to further clarify these points. We studied the sequential changes in the thymus of CBA mice infected with Plasmodium berghei ANKA, a model in which 60-90% of the infected animals develop cerebral malaria. During the acute phase of infection, different degrees of thymocyte apoptosis were recorded: (1) starry-sky pattern of diffuse apoptosis with maintenance of cortical-medullary structure; (2) intense apoptosis with cortical atrophy, with absence of large cells; (3) severe cortical thymocyte depletion, resulting in cortical-medullary inversion. In the latter, only residual clusters of small thymocytes were observed within the framework of epithelial cells. The intensity of thymus alterations could not be associated with the degree of parasitemia, the expression of clinical signs of cerebral malaria or intensity of brain lesions. The implications of these events for malaria immunity and pathology are discussed. |
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Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA micemalariathymusPlasmodium bergheimiceImmune responses to malaria infections are characterized by strong T and B cell activation, which, in addition of potentially causing immunopathology, are of poor efficacy against the infection. It is possible that the thymus is involved in the origin of immunopathological reactions and a target during malaria infections. This work was developed in an attempt to further clarify these points. We studied the sequential changes in the thymus of CBA mice infected with Plasmodium berghei ANKA, a model in which 60-90% of the infected animals develop cerebral malaria. During the acute phase of infection, different degrees of thymocyte apoptosis were recorded: (1) starry-sky pattern of diffuse apoptosis with maintenance of cortical-medullary structure; (2) intense apoptosis with cortical atrophy, with absence of large cells; (3) severe cortical thymocyte depletion, resulting in cortical-medullary inversion. In the latter, only residual clusters of small thymocytes were observed within the framework of epithelial cells. The intensity of thymus alterations could not be associated with the degree of parasitemia, the expression of clinical signs of cerebral malaria or intensity of brain lesions. The implications of these events for malaria immunity and pathology are discussed.Instituto Oswaldo Cruz, Ministério da Saúde2006-08-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://www.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762006000500007Memórias do Instituto Oswaldo Cruz v.101 n.5 2006reponame:Memórias do Instituto Oswaldo Cruzinstname:Fundação Oswaldo Cruzinstacron:FIOCRUZ10.1590/S0074-02762006000500007info:eu-repo/semantics/openAccessCarvalho,Leonardo JMFerreira-da-Cruz,Maria FDaniel-Ribeiro,Claudio TPelajo-Machado,MarceloLenzi,Henrique Leng2020-04-25T17:49:36Zhttp://www.scielo.br/oai/scielo-oai.php0074-02761678-8060opendoar:null2020-04-26 02:13:53.829Memórias do Instituto Oswaldo Cruz - Fundação Oswaldo Cruztrue |
dc.title.none.fl_str_mv |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
title |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
spellingShingle |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice Carvalho,Leonardo JM malaria thymus Plasmodium berghei mice |
title_short |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
title_full |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
title_fullStr |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
title_full_unstemmed |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
title_sort |
Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice |
author |
Carvalho,Leonardo JM |
author_facet |
Carvalho,Leonardo JM Ferreira-da-Cruz,Maria F Daniel-Ribeiro,Claudio T Pelajo-Machado,Marcelo Lenzi,Henrique L |
author_role |
author |
author2 |
Ferreira-da-Cruz,Maria F Daniel-Ribeiro,Claudio T Pelajo-Machado,Marcelo Lenzi,Henrique L |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Carvalho,Leonardo JM Ferreira-da-Cruz,Maria F Daniel-Ribeiro,Claudio T Pelajo-Machado,Marcelo Lenzi,Henrique L |
dc.subject.por.fl_str_mv |
malaria thymus Plasmodium berghei mice |
topic |
malaria thymus Plasmodium berghei mice |
dc.description.none.fl_txt_mv |
Immune responses to malaria infections are characterized by strong T and B cell activation, which, in addition of potentially causing immunopathology, are of poor efficacy against the infection. It is possible that the thymus is involved in the origin of immunopathological reactions and a target during malaria infections. This work was developed in an attempt to further clarify these points. We studied the sequential changes in the thymus of CBA mice infected with Plasmodium berghei ANKA, a model in which 60-90% of the infected animals develop cerebral malaria. During the acute phase of infection, different degrees of thymocyte apoptosis were recorded: (1) starry-sky pattern of diffuse apoptosis with maintenance of cortical-medullary structure; (2) intense apoptosis with cortical atrophy, with absence of large cells; (3) severe cortical thymocyte depletion, resulting in cortical-medullary inversion. In the latter, only residual clusters of small thymocytes were observed within the framework of epithelial cells. The intensity of thymus alterations could not be associated with the degree of parasitemia, the expression of clinical signs of cerebral malaria or intensity of brain lesions. The implications of these events for malaria immunity and pathology are discussed. |
description |
Immune responses to malaria infections are characterized by strong T and B cell activation, which, in addition of potentially causing immunopathology, are of poor efficacy against the infection. It is possible that the thymus is involved in the origin of immunopathological reactions and a target during malaria infections. This work was developed in an attempt to further clarify these points. We studied the sequential changes in the thymus of CBA mice infected with Plasmodium berghei ANKA, a model in which 60-90% of the infected animals develop cerebral malaria. During the acute phase of infection, different degrees of thymocyte apoptosis were recorded: (1) starry-sky pattern of diffuse apoptosis with maintenance of cortical-medullary structure; (2) intense apoptosis with cortical atrophy, with absence of large cells; (3) severe cortical thymocyte depletion, resulting in cortical-medullary inversion. In the latter, only residual clusters of small thymocytes were observed within the framework of epithelial cells. The intensity of thymus alterations could not be associated with the degree of parasitemia, the expression of clinical signs of cerebral malaria or intensity of brain lesions. The implications of these events for malaria immunity and pathology are discussed. |
publishDate |
2006 |
dc.date.none.fl_str_mv |
2006-08-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762006000500007 |
url |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762006000500007 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0074-02762006000500007 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Instituto Oswaldo Cruz, Ministério da Saúde |
publisher.none.fl_str_mv |
Instituto Oswaldo Cruz, Ministério da Saúde |
dc.source.none.fl_str_mv |
Memórias do Instituto Oswaldo Cruz v.101 n.5 2006 reponame:Memórias do Instituto Oswaldo Cruz instname:Fundação Oswaldo Cruz instacron:FIOCRUZ |
reponame_str |
Memórias do Instituto Oswaldo Cruz |
collection |
Memórias do Instituto Oswaldo Cruz |
instname_str |
Fundação Oswaldo Cruz |
instacron_str |
FIOCRUZ |
institution |
FIOCRUZ |
repository.name.fl_str_mv |
Memórias do Instituto Oswaldo Cruz - Fundação Oswaldo Cruz |
repository.mail.fl_str_mv |
|
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1669937697039319040 |