| Author | Barral Netto, Manoel | |
| Author | Silva, João Santana da | |
| Author | Barral, Aldina Maria Prado | |
| Author | Reed, Steven G | |
| Access date | 2014-05-13T14:27:31Z | |
| Available date | 2014-05-13T14:27:31Z | |
| Document date | 1995 | |
| Citation | BARRAL-NETTO, M. et al. Up-regulation of T helper 2 and down-regulation of T helper 1 cytokines during murine retrovirus-induced immunodeficiency syndrome enhances susceptibility of a resistant mouse strain to Leishmania amazonensis. American Journal of Pathology, v. 146, n. 3, p. 635-651, 1995. | pt_BR |
| ISSN | 0002-9440 | |
| URI | https://www.arca.fiocruz.br/handle/icict/7616 | |
| Language | eng | pt_BR |
| Publisher | American Association of Pathologists | pt_BR |
| Rights | open access | pt_BR |
| Subject in Portuguese | Leishmania | pt_BR |
| Subject in Portuguese | Citocinas | pt_BR |
| Subject in Portuguese | Macrófagos | pt_BR |
| Subject in Portuguese | Retrovírus | pt_BR |
| Subject in Portuguese | Infecção | pt_BR |
| Subject in Portuguese | Animais | pt_BR |
| Subject in Portuguese | Ratos | pt_BR |
| Subject in Portuguese | Camundongos | pt_BR |
| Title | Up-regulation of T helper 2 and down-regulation of T helper 1 cytokines during murine retrovirus-induced immunodeficiency syndrome enhances susceptibility of a resistant mouse strain to Leishmania amazonensis | pt_BR |
| Type | Article | pt_BR |
| Abstract | Resistance to and recovery from leishmania infection
is dependent on cell-mediated immunity.
C57BL/6 mice are resistant to Leishmania amazonensis
(La) infection but susceptible to LP-BM5
murine leukemia virus (MuLV) infection. MuLVinfection
leads to a state ofimmunodeficiency characterized
by severe compromise ofcell-mediated
immunity. When infected with La alone, C57BL/6
mice developed a smaU transient lesion that
evolved to spontaneous healing or a lesion with
extremely slow growth. Lesions were predominantly
comprised ofa lympho-macrophagic infiltrate
with few parasitized macrophages. When
infected with La and, 4 weeks later, with MuLV
(La-MuLV), the mice developed a large uncontrolled
nonhealing lesion containing vacuolated
and heavily parasitized macrophages. In contrast,
mice infected with MuLV first and La 4
weeks later (MuLV-La) developed a smaU butpersistent
lesion, characterized histologicaly by a
smaU number of heavily parasitized macrophages
andfew lympbocytes. Eight weeks after
MuLV infection, both had similar immunological
profiles with decreased lymphocyte proliferation,
diminished production ofinterferon-)y, and
high production of interleukins 4 and 10. At the
time of L. amazonensis infection, La-MuLV animals
have a normal T ceU function whereas in MuLV-La mice this function is already impaired,-
this may influence the recruitment of macrophages
to the site of leishmania injection. | pt_BR |
| Affilliation | Federal University of Bahia. School of Medicine. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil | pt_BR |
| Affilliation | Ribeiro Preto University of São Paulo. Ribeirão Preto, SP, Brasil | pt_BR |
| Affilliation | Federal University of Bahia. School of Medicine. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil | pt_BR |
| Affilliation | Seattle Biomedical Research Institute. Seattle, Washington | pt_BR |
