| Registro completo |
| Provedor de dados: |
BJMBR
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| País: |
Brazil
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| Título: |
The role of natural killer cells in the early period of infection in murine cutaneous leishmaniasis
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| Autores: |
Laurenti,M.D.
Gidlund,M.
Ura,D.M.
Sinhorini,I.L.
Corbett,C.E.P.
Goto,H.
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| Data: |
1999-03-01
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| Ano: |
1999
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| Palavras-chave: |
Cutaneous leishmaniasis
NK cells
Strontium 90
Leishmania (Leishmania) amazonensis
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| Resumo: |
In order to study the role of natural killer (NK) cells during the early period of Leishmania infection, BALB/c mice were selectively and permanently depleted of NK cells by injection with 90Sr and subsequently infected with Leishmania (Leishmania) amazonensis (HSJD-1 strain). 90Sr is known to selectively deplete NK cells, leaving an intact T- and B-cell compartment and preserving the ability to produce both interferon alpha and IL-2. This method of depletion has advantages when compared with depletion using anti-NK cell monoclonal antibodies because the effect is permanent and neither activates complement nor provokes massive cell death. In the present study, after one month of treatment with 90Sr, the depletion of NK cells was shown by a more than ten-fold reduction in the cytotoxic activity of these cells: 2 x 106 spleen cells from NK-depleted animals were required to reach the same specific lysis of target cells effected by 0.15 x 106 spleen cells from normal control animals. The histopathology of the skin lesion at 7 days after Leishmania infection showed more parasites in the NK cell-depleted group. This observation further strengthens a direct role of NK cells during the early period of Leishmania infection.
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| Tipo: |
Info:eu-repo/semantics/other
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000300012
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/S0100-879X1999000300012
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.32 n.3 1999
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| Direitos: |
info:eu-repo/semantics/openAccess
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