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How does the apicomplexan parasite Theileria control host cell identity?
Marsolier, Justine ; Weitzman, Jonathan B
Biologie aujourd'hui, 2014, Vol.208 (4), p.311
[Periódico revisado por pares]
France
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Título:
How does the apicomplexan parasite Theileria control host cell identity?
Autor:
Marsolier, Justine
;
Weitzman, Jonathan B
Assuntos:
Animals
;
Apoptosis
;
Arachnid Vectors - parasitology
;
Cattle
;
Cattle Diseases - parasitology
;
Cattle Diseases - pathology
;
Cell Transformation, Neoplastic
;
Enzyme Activation
;
Epigenesis, Genetic
;
Host-Parasite Interactions - physiology
;
Leukocytes, Mononuclear - parasitology
;
Life Cycle Stages
;
Lymphoproliferative Disorders - parasitology
;
Lymphoproliferative Disorders - pathology
;
Lymphoproliferative Disorders - veterinary
;
Macrophages - parasitology
;
MicroRNAs - genetics
;
NF-kappa B - physiology
;
Protein-Tyrosine Kinases - physiology
;
Salivary Glands - parasitology
;
Signal Transduction
;
Theileria - growth & development
;
Theileria - physiology
;
Theileriasis - parasitology
;
Theileriasis - pathology
;
Theileriasis - transmission
;
Ticks - parasitology
;
Transcription Factors - physiology
É parte de:
Biologie aujourd'hui, 2014, Vol.208 (4), p.311
Descrição:
Infectious agents, like bacteria or virus, are responsible for a large number of pathologies in mammals. Microbes have developed mechanisms for interacting with host cell pathways and hijacking cellular machinery to change the phenotypic state. In this review, we focus on an interesting apicomplexan parasite called Theileria. Infection by the tick-transmitted T. annulata parasite causes Tropical Theileriosis in North Africa and Asia, and the related T. parva parasite causes East Coast Fever in Sub-Saharan Africa. This parasite is the only eukaryote known to induce the transformation of its mammalian host cells. Indeed, T. annulata and T. parva infect bovine leukocytes leading to transforming phenotypes, which partially mirror human lymphoma pathologies. Theileria infection causes hyperproliferation, invasiveness and escape from apoptosis, presumably through the manipulation of host cellular pathways. Several host-signaling mechanisms have been implicated. Here we describe the mechanisms involved in parasite-induced transformation phenotypes.
Editor:
France
Idioma:
Francês
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