Data/hora: 13/06/2024 08:25:13

Provedor de dados: | 56
País: | Brazil
Título: | Relationship of cytokines and cytokine signaling to immunodeficiency disorders in the mouse
Autores: | Morawetz,R.A.; Giese,N.A.; Gabriele,L.; Rothman,P.; Horak,I.; Ozato,K.; Morse III,H.C.
Data: | 1998-01-01
Ano: | 1998
Palavras-chave: | ICSBP; Immunodeficiency; Interferon; MAIDS.
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-&lt;FONT FACE="Symbol"&gt;g&lt;/font&gt;, 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-&lt;FONT FACE="Symbol"&gt;g&lt;/font&gt; 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-&lt;FONT FACE="Symbol"&gt;g&lt;/font&gt; 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
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100008
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X1998000100008
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.31 n.1 1998
Fonte: | info:eu-repo/semantics/openAccess