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Book ; Thesis: Target discrimination during initiation of complement activation

Jokiranta, T. Sakari

1999

Author's details	T. Sakari Jokiranta
Language	English
Size	Getr. Zählung : graph. Darst.
Publishing country	Finland
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Helsinki, Univ., Diss., 1999
HBZ-ID	HT012884626
ISBN	952-91-1453-2 ; 978-952-91-1453-5
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: HUS and atypical HUS.

Jokiranta, T Sakari

Blood

2017 Volume 129, Issue 21, Page(s) 2847–2856

Abstract: Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kidney failure. HUS is usually categorized as typical, caused by Shiga toxin- ... ...

Abstract	Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kidney failure. HUS is usually categorized as typical, caused by Shiga toxin-producing
MeSH term(s)	Atypical Hemolytic Uremic Syndrome/blood ; Atypical Hemolytic Uremic Syndrome/genetics ; Atypical Hemolytic Uremic Syndrome/pathology ; Atypical Hemolytic Uremic Syndrome/therapy ; Complement Activation/genetics ; Diacylglycerol Kinase/blood ; Diacylglycerol Kinase/genetics ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Hemolysis ; Humans ; Platelet Activation ; Thrombosis/blood ; Thrombosis/genetics ; Thrombosis/pathology ; Thrombosis/therapy ; Vitamin B 12/blood
Chemical Substances	DGKE protein, human (EC 2.7.1.107) ; Diacylglycerol Kinase (EC 2.7.1.107) ; Vitamin B 12 (P6YC3EG204)
Language	English
Publishing date	2017-04-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2016-11-709865
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Assessing the Need for Multiplex and Multifunctional Tick-Borne Disease Test in Routine Clinical Laboratory Samples from Lyme Disease and Febrile Patients with a History of a Tick Bite.

Garg, Kunal / Jokiranta, T Sakari / Filén, Sanna / Gilbert, Leona

Tropical medicine and infectious disease

2021 Volume 6, Issue 1

Abstract: Human polymicrobial infections in tick-borne disease (TBD) patients is an emerging public health theme. However, the requirement for holistic TBD tests in routine clinical laboratories is ambiguous. ... ...

Abstract	Human polymicrobial infections in tick-borne disease (TBD) patients is an emerging public health theme. However, the requirement for holistic TBD tests in routine clinical laboratories is ambiguous. TICKPLEX
Language	English
Publishing date	2021-03-17
Publishing country	Switzerland
Document type	Journal Article
ISSN	2414-6366
ISSN (online)	2414-6366
DOI	10.3390/tropicalmed6010038
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Assessing the Need for Multiplex and Multifunctional Tick-Borne Disease Test in Routine Clinical Laboratory Samples from Lyme Disease and Febrile Patients with a History of a Tick Bite

Kunal Garg / T. Sakari Jokiranta / Sanna Filén / Leona Gilbert

Tropical Medicine and Infectious Disease, Vol 6, Iss 38, p

2021 Volume 38

Abstract	Human polymicrobial infections in tick-borne disease (TBD) patients is an emerging public health theme. However, the requirement for holistic TBD tests in routine clinical laboratories is ambiguous. TICKPLEX ® PLUS is a holistic TBD test utilized herein to assess the need for multiplex and multifunctional diagnostic tools in a routine clinical laboratory. The study involved 150 specimens categorized into Lyme disease (LD)-positive ( n = 48), LD-negative ( n = 30), and febrile patients from whom borrelia serology was requested ( n = 72, later “febrile patients”) based on reference test results from United Medix, Finland. Reference tests from DiaSorin, Immunetics, and Mikrogen Diagnostik followed the two-tier LD testing system. A comparison between the reference tests and TICKPLEX ® PLUS produced 86%, 88%, and 87% positive, negative, and overall agreement, respectively. Additionally, up to 15% of LD and 11% of febrile patients responded to TBD related coinfections and opportunistic microbes. The results demonstrated that one (TICKPLEX ® PLUS) test can aid in a LD diagnosis instead of four tests. Moreover, TBD is not limited to just LD, as the specimens produced immune responses to several TBD microbes. Lastly, the study indicated that the screening of febrile patients for TBDs could be a missed opportunity at reducing unreported patient cases.
Keywords	Lyme disease ; tick-borne disease ; zoonoses ; spirochetes ; polymicrobial ; summer flu ; Medicine ; R
Subject code	610
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Benefit of measuring vedolizumab concentrations in inflammatory bowel disease patients in a real-world setting.

Kolehmainen, Sara / Ylisaukko-Oja, Tero / Jokelainen, Jari / Koivusalo, Mirkka / Jokiranta, T Sakari / Sipponen, Taina

Scandinavian journal of gastroenterology

2021 Volume 56, Issue 8, Page(s) 906–913

Abstract: Objectives: We set out to determine the reasons for serum vedolizumab (VDZ) trough concentration (TC) measurements in inflammatory bowel disease (IBD) patients and to evaluate treatment modifications after therapeutic drug measurement (TDM). We also ... ...

Abstract	Objectives: We set out to determine the reasons for serum vedolizumab (VDZ) trough concentration (TC) measurements in inflammatory bowel disease (IBD) patients and to evaluate treatment modifications after therapeutic drug measurement (TDM). We also evaluated the effect of increased dosing on patients' response to VDZ therapy. Methods: We performed a retrospective cohort study of IBD patients who received VDZ therapy at Helsinki University Hospital and whose VDZ levels were measured between June 2014 and December 2018. Results: Altogether, 90 patients (32 Crohn's disease and 58 ulcerative colitis) and 141 VDZ TC measurements were included. 24.1% of measurements took place during induction and 75.9% during the maintenance phase. During induction, 64.7% reached the target TC >20µg/ml. During maintenance therapy, 82.2% of VDZ TCs were within or exceeded the suggested target range of 5-15µg/ml. Reasons for TDM were: secondary nonresponse (44.0%), assessment of adequate VDZ TC (25.5%), primary nonresponse (12.8%), adverse events (6.4%), and other (11.3%). No treatment changes occurred after 60.3% of VDZ measurements. Increased dose frequency was used after 25.5% of VDZ measurements and 33.3% of these patients experienced improvement. Altogether, 31 (34.4%) patients discontinued the therapy due to inadequate treatment response. No anti-vedolizumab antibodies were detected. Conclusions: During the maintenance of VDZ therapy, the majority of VDZ TCs were within the suggested range. Measurement of VDZ TC did not lead to any treatment changes in two-thirds of patients. Dose optimization occurred in a quarter of patients and a third of them benefited from it.
MeSH term(s)	Antibodies, Monoclonal, Humanized/therapeutic use ; Colitis, Ulcerative/drug therapy ; Gastrointestinal Agents/therapeutic use ; Humans ; Inflammatory Bowel Diseases/drug therapy ; Retrospective Studies
Chemical Substances	Antibodies, Monoclonal, Humanized ; Gastrointestinal Agents ; vedolizumab (9RV78Q2002)
Language	English
Publishing date	2021-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	82042-8
ISSN	1502-7708 ; 0036-5521
ISSN (online)	1502-7708
ISSN	0036-5521
DOI	10.1080/00365521.2021.1938206
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Minor Role of Plasminogen in Complement Activation on Cell Surfaces.

Hyvärinen, Satu / Jokiranta, T Sakari

PloS one

2015 Volume 10, Issue 12, Page(s) e0143707

Abstract: Atypical hemolytic uremic syndrome (aHUS) is a rare, but severe thrombotic microangiopathy. In roughly two thirds of the patients, mutations in complement genes lead to uncontrolled activation of the complement system against self cells. Recently, aHUS ... ...

Abstract	Atypical hemolytic uremic syndrome (aHUS) is a rare, but severe thrombotic microangiopathy. In roughly two thirds of the patients, mutations in complement genes lead to uncontrolled activation of the complement system against self cells. Recently, aHUS patients were described with deficiency of the fibrinolytic protein plasminogen. This zymogen and its protease form plasmin have both been shown to interact with complement proteins in the fluid phase. In this work we studied the potential of plasminogen to restrict complement propagation. In hemolytic assays, plasminogen inhibited complement activation, but only when it had been exogenously activated to plasmin and when it was used at disproportionately high concentrations compared to serum. Addition of only the zymogen plasminogen into serum did not hinder complement-mediated lysis of erythrocytes. Plasminogen could not restrict deposition of complement activation products on endothelial cells either, as was shown with flow cytometry. With platelets, a very weak inhibitory effect on deposition of C3 fragments was observed, but it was considered too weak to be significant for disease pathogenesis. Thus it was concluded that plasminogen is not an important regulator of complement on self cells. Instead, addition of plasminogen was shown to clearly hinder platelet aggregation in serum. This was attributed to plasmin causing disintegration of formed platelet aggregates. We propose that reduced proteolytic activity of plasmin on structures of growing thrombi, rather than on complement activation fragments, explains the association of plasminogen deficiency with aHUS. This adds to the emerging view that factors unrelated to the complement system can also be central to aHUS pathogenesis and suggests that future research on the mechanism of the disease should expand beyond complement dysregulation.
MeSH term(s)	Blood Platelets/metabolism ; Blood Platelets/pathology ; Complement Activation ; Erythrocytes/metabolism ; Erythrocytes/pathology ; Female ; Fibrinolysin/metabolism ; Hemolysis ; Hemolytic-Uremic Syndrome/metabolism ; Hemolytic-Uremic Syndrome/pathology ; Humans ; Male ; Plasminogen/metabolism ; Platelet Aggregation ; Proteolysis
Chemical Substances	Plasminogen (9001-91-6) ; Fibrinolysin (EC 3.4.21.7)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0143707
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Minor Role of Plasminogen in Complement Activation on Cell Surfaces.

Satu Hyvärinen / T Sakari Jokiranta

PLoS ONE, Vol 10, Iss 12, p e

2015 Volume 0143707

Abstract	Atypical hemolytic uremic syndrome (aHUS) is a rare, but severe thrombotic microangiopathy. In roughly two thirds of the patients, mutations in complement genes lead to uncontrolled activation of the complement system against self cells. Recently, aHUS patients were described with deficiency of the fibrinolytic protein plasminogen. This zymogen and its protease form plasmin have both been shown to interact with complement proteins in the fluid phase. In this work we studied the potential of plasminogen to restrict complement propagation. In hemolytic assays, plasminogen inhibited complement activation, but only when it had been exogenously activated to plasmin and when it was used at disproportionately high concentrations compared to serum. Addition of only the zymogen plasminogen into serum did not hinder complement-mediated lysis of erythrocytes. Plasminogen could not restrict deposition of complement activation products on endothelial cells either, as was shown with flow cytometry. With platelets, a very weak inhibitory effect on deposition of C3 fragments was observed, but it was considered too weak to be significant for disease pathogenesis. Thus it was concluded that plasminogen is not an important regulator of complement on self cells. Instead, addition of plasminogen was shown to clearly hinder platelet aggregation in serum. This was attributed to plasmin causing disintegration of formed platelet aggregates. We propose that reduced proteolytic activity of plasmin on structures of growing thrombi, rather than on complement activation fragments, explains the association of plasminogen deficiency with aHUS. This adds to the emerging view that factors unrelated to the complement system can also be central to aHUS pathogenesis and suggests that future research on the mechanism of the disease should expand beyond complement dysregulation.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Disturbed sialic acid recognition on endothelial cells and platelets in complement attack causes atypical hemolytic uremic syndrome.

Hyvärinen, Satu / Meri, Seppo / Jokiranta, T Sakari

Blood

2016 Volume 127, Issue 22, Page(s) 2701–2710

Abstract: Uncontrolled activation of the complement system against endothelial and blood cells is central to the pathogenesis of atypical hemolytic uremic syndrome (aHUS). aHUS patients frequently carry mutations in the inhibitory complement regulator factor H (FH) ...

Abstract	Uncontrolled activation of the complement system against endothelial and blood cells is central to the pathogenesis of atypical hemolytic uremic syndrome (aHUS). aHUS patients frequently carry mutations in the inhibitory complement regulator factor H (FH). Mutations cluster in domains 19 and 20 (FH19-20), which are critical for recognizing self surfaces. On endothelial cells, binding of FH is generally attributed to heparan sulfate. This theory, however, is questioned by the puzzling observation that some aHUS-associated mutations markedly enhance FH binding to heparin and endothelial cells. In this article, we show that, instead of disturbed heparin interactions, the impaired ability of C-terminal mutant FH molecules to recognize sialic acid in the context of surface-bound C3b explains their pathogenicity. By using recombinant FH19-20 as a competitor for FH and measuring erythrocyte lysis and deposition of complement C3b and C5b-9 on endothelial cells and platelets, we now show that several aHUS-associated mutations, which have been predicted to impair FH19-20 binding to sialic acid, prevent FH19-20 from antagonizing FH function on cells. When sialic acid was removed, the wild-type FH19-20 also lost its ability to interfere with FH function on cells. These results indicate that sialic acid is critical for FH-mediated complement regulation on erythrocytes, endothelial cells, and platelets. The inability of C-terminal mutant FH molecules to simultaneously bind sialic acid and C3b on cells provides a unifying explanation for their association with aHUS. Proper formation of FH-sialic acid-C3b complexes on surfaces exposed to plasma is essential for preventing cell damage and thrombogenesis characteristic of aHUS.
MeSH term(s)	Amino Acid Substitution ; Atypical Hemolytic Uremic Syndrome/genetics ; Atypical Hemolytic Uremic Syndrome/metabolism ; Binding Sites ; Blood Platelets ; Complement C3b/chemistry ; Complement C3b/metabolism ; Complement Factor H/chemistry ; Complement Factor H/genetics ; Complement Factor H/metabolism ; Complement Membrane Attack Complex/chemistry ; Complement Membrane Attack Complex/metabolism ; Endothelial Cells ; Humans ; Mutation, Missense ; N-Acetylneuraminic Acid/chemistry ; N-Acetylneuraminic Acid/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism
Chemical Substances	Complement Membrane Attack Complex ; Recombinant Proteins ; Complement C3b (80295-43-8) ; Complement Factor H (80295-65-4) ; N-Acetylneuraminic Acid (GZP2782OP0)
Language	English
Publishing date	2016-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2015-11-680009
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: C3b and factor H: key components of the complement system.

Jokiranta, T Sakari

Expert review of clinical immunology

2006 Volume 2, Issue 5, Page(s) 775–786

Abstract: In all three complement pathways, the central molecule is C3, which, upon activation cleavage, forms the major opsonin C3b - the key component of complement. C3b is also essential for propagation of the complement cascade to the stage of the lytic ... ...

Abstract	In all three complement pathways, the central molecule is C3, which, upon activation cleavage, forms the major opsonin C3b - the key component of complement. C3b is also essential for propagation of the complement cascade to the stage of the lytic terminal complement complexes. In order to prevent damage to self cells and tissues and restrict overconsumption of the complement components, C3b molecules need to be controlled by factor H. Defect in C3 functions leads to compromised microbial defence and increased susceptibility to certain autoimmune diseases. Deficiency of factor H, or a functional defect in its N terminus, often leads to membranoproliferative glomerulonephritis and complement depletion, owing to continuous overconsumption of C3. Defect in the factor H C terminus leads to a dramatically increased risk of atypical hemolytic uremic syndrome. In addition, recently, a polymorphism in the middle part of factor H (Y402H) has been shown to be the major risk factor for the most common cause of blindness in the industrialized world: age-related macular degeneration. In future, analysis of patient samples for defects in these key complement components may prove useful in diagnosis of these diseases and new therapeutic targets will certainly be the aim for use in the recently recognized factor H-related diseases.
Language	English
Publishing date	2006-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2274260-8
ISSN	1744-8409 ; 1744-666X
ISSN (online)	1744-8409
ISSN	1744-666X
DOI	10.1586/1744666X.2.5.775
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Article ; Online: Dientamoeba fragilis

Pietilä, Jukka-Pekka / Meri, Taru / Siikamäki, Heli / Tyyni, Elisabet / Kerttula, Anne-Marie / Pakarinen, Laura / Jokiranta, T Sakari / Kantele, Anu

Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin

2019 Volume 24, Issue 29

Abstract: BackgroundDespite the global distribution of the intestinal ... ...

Abstract	BackgroundDespite the global distribution of the intestinal protozoan
MeSH term(s)	Abdominal Pain ; Adult ; Animals ; Diarrhea/parasitology ; Dientamoeba/genetics ; Dientamoeba/isolation & purification ; Dientamoebiasis/epidemiology ; Dientamoebiasis/parasitology ; Dientamoebiasis/transmission ; Feces/parasitology ; Female ; Finland/epidemiology ; Giardiasis/epidemiology ; Humans ; Male ; Middle Aged ; Polymerase Chain Reaction ; Retrospective Studies ; Sex Distribution
Language	English
Publishing date	2019-07-24
Publishing country	Sweden
Document type	Journal Article
ZDB-ID	1338803-4
ISSN	1560-7917 ; 1025-496X
ISSN (online)	1560-7917
ISSN	1025-496X
DOI	10.2807/1560-7917.ES.2019.24.29.1800546
Database	MEDical Literature Analysis and Retrieval System OnLINE

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