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E-GEOD-52624 - Leishmania major modulates autophagy in host macrophages during intracellular differentiation

Released on 3 August 2015, last updated on 19 August 2015
Mus musculus
Samples (8)
Array (1)
Protocols (7)
Autophagy generally participates in innate immunity by elimination of intracellular pathogens. However, many of them developed successful strategies to counteract their autolysosomal digestion and lastly to exploit this catabolic cellular process. Protozoan parasites of the genus Leishmania are the causative agent of leishmaniasis, one of the 13 most important tropical diseases. Leishmania persists as endo-parasite in host macrophages, where it uses multiple strategies to manipulate the microbicidal host cell functions and to escape from the host immune system. Understanding how Leishmania interacts with host macrophages during uptake, differentiation, intracellular replication, and release might be the key to develop new drugs in target-directed approaches to treat patient with leishmaniasis. Here, we generated expression profiles from bone marrow-derived macrophages (BMDM) at 1h and 24h post infection (p.i.) with Leishmania major and respective controls.
Experiment type
transcription profiling by array 
Claus Juergen Scholz <>, Benjamin Frank, Claus J Scholz, Heike Weber, Uta Schurigt
Autophagic digestion of Leishmania major by host macrophages is associated with differential expression of BNIP3, CTSE, and the miRNAs miR-101c, miR-129, and miR-210. Frank B, Marcu A, de Oliveira Almeida Petersen AL, Weber H, Stigloher C, Mottram JC, Scholz CJ, Schurigt U.
Investigation descriptionE-GEOD-52624.idf.txt
Sample and data relationshipE-GEOD-52624.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-AFFY-45.adf.txt