PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31748116-1	2020	Galactose-deficient IgA1 (Gd-IgA1) plays a crucial role in the development of IgA nephropathy (IgAN).	Gadolinium	26-28	immunoglobulin heavy constant alpha 1	Homo sapiens	20-24	
31748116-1	2020	Galactose-deficient IgA1 (Gd-IgA1) plays a crucial role in the development of IgA nephropathy (IgAN).	Gadolinium	26-28	immunoglobulin heavy constant alpha 1	Homo sapiens	29-33	
31748116-2	2020	However, the pathogenic mechanisms driving Gd-IgA1 production have not been fully elucidated.	Gadolinium	43-45	immunoglobulin heavy constant alpha 1	Homo sapiens	46-50	
31748116-3	2020	Innate-immune activation via Toll-like receptor 9 (TLR9) is known to be involved in Gd-IgA1 production.	Gadolinium	84-86	immunoglobulin heavy constant alpha 1	Homo sapiens	87-91	
31748116-4	2020	A proliferation inducing ligand (APRIL) and IL-6 are also known to enhance Gd-IgA1 synthesis in IgAN.	Gadolinium	75-77	immunoglobulin heavy constant alpha 1	Homo sapiens	78-82	
31748116-9	2020	However, siRNA knock-down of APRIL completely suppressed overproduction of Gd-IgA1 induced by IL-6.	Gadolinium	75-77	immunoglobulin heavy constant alpha 1	Homo sapiens	78-82	
31748116-10	2020	Neutralization of IL-6 decreased CpG-oligonucleotide-induced overproduction of Gd-IgA1.	Gadolinium	79-81	immunoglobulin heavy constant alpha 1	Homo sapiens	82-86	
31748116-11	2020	Furthermore, APRIL and IL-6 pathways each independently mediated TLR9-induced overproduction of Gd-IgA1.	Gadolinium	96-98	immunoglobulin heavy constant alpha 1	Homo sapiens	99-103	
31748116-13	2020	Hence, APRIL and IL-6 synergistically, as well as independently, enhance synthesis of Gd-IgA1.	Gadolinium	86-88	immunoglobulin heavy constant alpha 1	Homo sapiens	89-93