PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29066027-7	2018	ADA positive patients showed higher T cell responses to IFN-beta protein than ADA negative patients and untreated controls.	N-(2-acetamido)iminodiacetic acid	0-3	interferon beta 1	Homo sapiens	56-64	
33143745-2	2020	Up to 40% of multiple sclerosis patients treated with interferon beta (IFNbeta) develop ADA, for which a genetic predisposition exists.	N-(2-acetamido)iminodiacetic acid	88-91	interferon beta 1	Homo sapiens	54-69	
29066027-7	2018	ADA positive patients showed higher T cell responses to IFN-beta protein than ADA negative patients and untreated controls.	N-(2-acetamido)iminodiacetic acid	78-81	interferon beta 1	Homo sapiens	56-64	
28729851-3	2017	Screening assay: ADA in serum samples form complexes with immobilized IFN-beta and biotinylated IFN-beta, which are then detected using HRP labeled Streptavidin and TMB substrate.	N-(2-acetamido)iminodiacetic acid	17-20	interferon beta 1	Homo sapiens	70-78	
28729851-3	2017	Screening assay: ADA in serum samples form complexes with immobilized IFN-beta and biotinylated IFN-beta, which are then detected using HRP labeled Streptavidin and TMB substrate.	N-(2-acetamido)iminodiacetic acid	17-20	interferon beta 1	Homo sapiens	96-104	
28418769-6	2017	Persistency of neutralizing ADA was predicted by their titers at month 24 and month 36 of treatment and by an increase of antibody affinity within the second year of IFN-beta treatment.	N-(2-acetamido)iminodiacetic acid	28-31	interferon beta 1	Homo sapiens	166-174	
28418769-7	2017	The humoral immune response to IFN-beta observed in MS patients as a result of IFN-beta therapy is a multifactorial process that is influenced by ADA titers, affinity maturation, and IgG subclass switching.	N-(2-acetamido)iminodiacetic acid	146-149	interferon beta 1	Homo sapiens	31-39	
28418769-7	2017	The humoral immune response to IFN-beta observed in MS patients as a result of IFN-beta therapy is a multifactorial process that is influenced by ADA titers, affinity maturation, and IgG subclass switching.	N-(2-acetamido)iminodiacetic acid	146-149	interferon beta 1	Homo sapiens	79-87	
27806057-5	2016	In multivariate Cox regression, IFNbeta-1a subcutaneous and IFNbeta-1b subcutaneous treated patients were at higher risk of ADA occurrence compared to IFNbeta-1a intramuscular-treated patients (pooled HR = 6.4, 95% CI 4.9-8.4 and pooled HR = 8.7, 95% CI 6.6-11.4 respectively).	N-(2-acetamido)iminodiacetic acid	124-127	interferon beta 1	Homo sapiens	32-39	
27806057-5	2016	In multivariate Cox regression, IFNbeta-1a subcutaneous and IFNbeta-1b subcutaneous treated patients were at higher risk of ADA occurrence compared to IFNbeta-1a intramuscular-treated patients (pooled HR = 6.4, 95% CI 4.9-8.4 and pooled HR = 8.7, 95% CI 6.6-11.4 respectively).	N-(2-acetamido)iminodiacetic acid	124-127	interferon beta 1	Homo sapiens	60-67	
27806057-5	2016	In multivariate Cox regression, IFNbeta-1a subcutaneous and IFNbeta-1b subcutaneous treated patients were at higher risk of ADA occurrence compared to IFNbeta-1a intramuscular-treated patients (pooled HR = 6.4, 95% CI 4.9-8.4 and pooled HR = 8.7, 95% CI 6.6-11.4 respectively).	N-(2-acetamido)iminodiacetic acid	124-127	interferon beta 1	Homo sapiens	60-67	
27806057-8	2016	Interestingly we observed that in Sweden and Germany, patients who started IFNbeta in April were at higher risk of developing ADA (HR = 1.6, 95% CI 1.1-2.4 and HR = 2.4, 95% CI 1.5-3.9 respectively).	N-(2-acetamido)iminodiacetic acid	126-129	interferon beta 1	Homo sapiens	75-82	
23770627-8	2013	ADA interaction with therapeutic IFNbeta results in immune complex formation and complement activation.	N-(2-acetamido)iminodiacetic acid	0-3	interferon beta 1	Homo sapiens	33-40