Data/hora: 06/06/2024 11:41:05

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