PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25674053-12	2015	These results suggest that microglial activation plays a critical role in the development of IFN-alpha-induced depression, and that minocycline is a promising drug for the treatment of IFN-alpha-induced depression in patients, especially those who are low responders to conventional antidepressant treatments.	Minocycline	132-143	interferon alpha 1	Homo sapiens	93-102	
24732038-5	2014	We found that minocycline attenuated in vitro induction of type I interferon (IFN) and the IFN-stimulated genes indoleamine 2,3-dioxygenase (IDO1) and TNF-related apoptosis inducing ligand (TRAIL) in human plasmacytoid dendritic cells and PBMCs exposed to aldrithiol-2 inactivated HIV or infectious influenza virus.	Minocycline	14-25	interferon alpha 1	Homo sapiens	59-82	
24732038-5	2014	We found that minocycline attenuated in vitro induction of type I interferon (IFN) and the IFN-stimulated genes indoleamine 2,3-dioxygenase (IDO1) and TNF-related apoptosis inducing ligand (TRAIL) in human plasmacytoid dendritic cells and PBMCs exposed to aldrithiol-2 inactivated HIV or infectious influenza virus.	Minocycline	14-25	interferon alpha 1	Homo sapiens	78-81	
24732038-9	2014	These results show that minocycline administered after infection may protect against aspects of activation-induced cell death during HIV/SIV immune disease, but that in vitro effects of minocycline on type I IFN responses are not recapitulated in a rapid progressor model in vivo.	Minocycline	186-197	interferon alpha 1	Homo sapiens	208-211	
27357391-9	2016	We also administrated minocycline, a microglial activation inhibitor, before the IFN-alpha infusion to testify the possibility to reverse the IFN-alpha-induced effects.	Minocycline	22-33	interferon alpha 1	Homo sapiens	142-151	
27357391-11	2016	Administering minocycline prevented IFN-alpha from impairing fear extinction.	Minocycline	14-25	interferon alpha 1	Homo sapiens	36-45	
27357391-12	2016	The immunohistochemical and biochemical results show that minocycline inhibited IFN-alpha-induced microglial activation and reduced IL-1beta and TNF-alpha production.	Minocycline	58-69	interferon alpha 1	Homo sapiens	80-89	
25674053-12	2015	These results suggest that microglial activation plays a critical role in the development of IFN-alpha-induced depression, and that minocycline is a promising drug for the treatment of IFN-alpha-induced depression in patients, especially those who are low responders to conventional antidepressant treatments.	Minocycline	132-143	interferon alpha 1	Homo sapiens	185-194