| Registro completo |
| Provedor de dados: |
BJMBR
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| País: |
Brazil
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| Título: |
Relationship of cytokines and cytokine signaling to immunodeficiency disorders in the mouse
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| Autores: |
Morawetz,R.A.
Giese,N.A.
Gabriele,L.
Rothman,P.
Horak,I.
Ozato,K.
Morse III,H.C.
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| Data: |
1998-01-01
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| Ano: |
1998
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| Palavras-chave: |
ICSBP
Immunodeficiency
Interferon
MAIDS
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| Resumo: |
The contributions of cytokines to the development and progression of disease in a mouse model of retrovirus-induced immunodeficiency (MAIDS) are controversial. Some studies have indicated an etiologic role for type 2 cytokines, while others have emphasized the importance of type 1 cytokines. We have used mice deficient in expression of IL-4, IL-10, IL-4 and IL-10, IFN-<FONT FACE="Symbol">g</font>, or ICSBP - a transcriptional protein involved in IFN signaling - to examine their contributions to this disorder. Our results demonstrate that expression of type 2 cytokines is an epiphenomenon of infection and that IFN-<FONT FACE="Symbol">g</font> is a driving force in disease progression. In addition, exogenously administered IL-12 prevents many manifestations of disease while blocking retrovirus expression. Interruption of the IFN signaling pathways in ICSBP-/- mice blocks induction of MAIDS. Predictably, ICSBP-deficient mice exhibit impaired responses to challenge with several other viruses. This immunodeficiency is associated with impaired production of IFN-<FONT FACE="Symbol">g</font> and IL-12. Unexpectedly, however, the ICSBP-/- mice also develop a syndrome with many similarities to chronic myelogenous leukemia in humans. The chronic phase of this disease is followed by a fatal blast crisis characterized by clonal expansions of undifferentiated cells. ICSBP is thus an important determinant of hematopoietic growth and differentiation as well as a prominent signaling molecule for IFNs
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100008
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/S0100-879X1998000100008
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.31 n.1 1998
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| Direitos: |
info:eu-repo/semantics/openAccess
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