Publications by authors named "Jensenius J"

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  • The study examines how in utero adversities like hypoxia and malnutrition relate to the development of schizophrenia (SZ) by investigating specific proteins (l-ficolin and MASP-2) linked to the immune response in patients.
  • Results show that SZ patients had significantly higher levels of l-ficolin (about 40% increase) and a notable gender difference in MASP-2 levels, especially among female patients.
  • The study also notes that while there are increases in certain protein activities in SZ, there was no significant association with demographic factors like age, family history, or smoking habits.
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  • * Researchers analyzed 122 IS patients and 150 controls using immunofluorometric assays and real-time PCR, finding significantly higher M-ficolin levels in IS patients and identifying several SNPs that negatively correlate with IS risk.
  • * The findings suggest that changes in LCP PRMs may influence the risk and progression of ischemic stroke, highlighting the role of genetic and protein level alterations in the disease mechanisms, especially in the Armenian population studied.
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  • There are various methods for detecting complement activation products, but no universal standard exists for clinical measurement.
  • The text outlines a modified assay for measuring C3dg, which is a component related to complement activation.
  • This modified assay is highlighted as simple, inexpensive, and stable, providing an accurate reflection of complement turnover regardless of the activation pathway.
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  • The study investigates the role of natural antibodies, specifically anti-αGal, in defending against pneumococcal infections caused by Streptococcus pneumoniae.
  • Researchers found that anti-αGal antibodies, despite not specifically targeting the known pneumococcal capsular types, can react with a significant number of pneumococcal serotypes and aid in microbial detection.
  • Evidence shows that higher levels of anti-αGal are linked to lower rates of pneumococcal infections, suggesting that these antibodies play a crucial role in enhancing human immunity against a variety of pathogens.
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  • Researchers studied the levels of ficolins and mannose-binding lectin (MBL) in 157 patients with acute myeloid leukaemia (AML) compared to 267 healthy individuals.
  • They found that ficolin-1 was significantly lower in AML patients, while ficolin-2, ficolin-3, and MBL were higher, with the highest MBL levels linked to a greater risk of severe infections.
  • Genotyping suggested a specific genetic variant (G/G homozygosity) associated with the disease, and ficolins could serve as potential new biomarkers for diagnosing AML and distinguishing it from other blood cancers.
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  • Some human antibodies, like IgG anti-αGal, can paradoxically inhibit complement activation on bacteria, potentially aiding pathogen survival!
  • A study using flow cytometry showed that IgG anti-αGal activates the classical complement pathway on various target cells, with activation levels dependent on antibody binding density!
  • The research challenges previous claims of inhibition, suggesting that earlier findings may have stemmed from inadequate experimental setups rather than an inherent inability of IgG anti-αGal to activate complement.
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  • The study investigates the roles of MASP-1, MASP-3, and MAp44 proteins in leprosy, highlighting their potential impact on enhancing phagocytosis of Mycobacterium leprae through the lectin pathway of complement.
  • Researchers analyzed five genetic variations in MASP1 among 196 leprosy patients and 193 controls, finding significant differences in serum levels of MASP-3 and MAp44 between these groups.
  • Results suggest that specific genetic variants may influence susceptibility to leprosy by regulating serum levels of these proteins, emphasizing the importance of the lectin pathway in immune response to infections.
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  • Research reexamined the role of IgG anti-αGal antibodies in human plasma, which are abundant and known to bind to bacteria causing sepsis.
  • Using purification techniques, the study characterized these antibodies and tested their reactivity against 100 clinical isolates from sepsis patients.
  • Findings show that IgG anti-αGal has high specificity for Galα3Gal and can bind to a significant number of pathogens, particularly Gram-positive bacteria, despite constituting a small fraction of the antibody pool.
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  • A study involving 312 patients with multiple myeloma and lymphomas assessed the levels of ficolins (immune proteins) and their genetic polymorphisms before and after high-dose chemotherapy and stem cell transplantation.
  • Findings showed that multiple myeloma patients had significantly lower levels of ficolin-1 and ficolin-2 compared to healthy controls, suggesting a link to the disease itself rather than post-transplant complications.
  • Genetic variations in the ficolin genes were more frequently found in cancer patients, with some polymorphisms associated with a higher risk of infections post-chemotherapy, especially in lymphoma patients.
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  • * Higher numbers of certain genetic variants (MBL2 gene exon 1) were found in tuberculosis patients compared to healthy individuals, while some variations (SFTPA2 +26 C > A SNP) were less common in patients.
  • * Increased levels of specific serum proteins, including ficolin-1, were seen in patients, suggesting ficolin-1 could be a potential marker to distinguish between tuberculosis patients and healthy individuals.
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  • Congenital heart disease (CHD) often requires surgery and can lead to serious post-operative complications, prompting a study on the innate immune system factors related to these outcomes in pediatric patients.
  • Key findings reveal that low levels of MAp44 are linked to increased complications like low cardiac output syndrome and renal issues, while low MASP-3 and high MASP-1 levels correlate with fatal outcomes.
  • Low ficolin-3 levels are associated with more severe complications, but surprisingly, patients with low ficolin-3 still had a much higher survival rate compared to others, suggesting its potential as a prognostic marker for post-operative recovery.
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MBL-associated serine proteases (MASP-1, MASP-2, MASP-3, MAp-44, and MAp-19) are key factors in the activation of the lectin pathway of complement. Serum levels of these components have been associated with recurrence and poor survival of some types of cancer, such as colorectal and ovarian cancer. In this investigation, we determined the serum levels of MASP-1, MASP-2, MASP-3, MAp-44, and MAp-19 in patients with cervical cancer and cervical intraepithelial neoplasia (CIN).

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  • The complement system is an important part of the immune system that helps detect and eliminate infectious agents by activating different pathways to mediate processes like cell lysis and opsonization.
  • The study focused on two proteins, Ficolin-1 and Ficolin-3, examining their plasma levels in HIV patients, both with and without co-infection with HCV, compared to healthy controls.
  • Results indicated lower levels of Ficolin-1 in HIV/HCV co-infected patients compared to both HIV-only patients and controls, while Ficolin-3 levels were higher in HIV patients compared to controls, with specific correlations noted for Ficolin-3 and T CD4 cell counts.
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  • - This study involved 312 patients with multiple myeloma and lymphomas undergoing high-dose chemotherapy and autologous stem cell transplantation, examining the role of certain gene polymorphisms and serum concentrations of immune-related proteins.
  • - Findings indicated that multiple myeloma patients had a higher prevalence of MBL deficiency genotypes, but this was not linked to hospital infections or recovery of white blood cells, although it correlated with more severe infections during follow-up.
  • - Interestingly, high levels of MBL were associated with prolonged fever and some infections post-chemotherapy, while a notable association between a gene mutation and lymphoma was identified, and overall, the influence of MBL on infections in these patients remains conflicting.
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  • The study investigates the role of the lectin pathway (LP) of complement activation in the pathogenesis of systemic lupus erythematosus (SLE), building on existing knowledge of the classical pathway (CP).
  • Researchers analyzed LP protein concentrations in 372 SLE patients and 170 controls, finding that LP proteins were altered in SLE and associated with decreased total complement C3 levels and disease activity.
  • The findings suggest that the LP is actively involved in SLE, with specific LP protein changes correlating with disease severity and complement activation, highlighting its potential role in the disease's progression.
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  • In 2012, hypocomplementemia was added to the criteria for diagnosing systemic lupus erythematosus (SLE), but measuring C3 or C4 is not very effective in tracking disease activity.
  • The study developed a new assay to measure C3dg, a fragment produced during complement activation, by separating it from larger proteins using polyethylene glycol (PEG), testing it on a group of SLE patients and controls.
  • Results indicated that C3dg levels were significantly higher in SLE patients, and the new assay was more effective than traditional C3 measurements in distinguishing between SLE patients and healthy controls, suggesting its inclusion in SLE classification criteria.
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  • * A study highlights the role of the complement inhibitor mannan-binding lectin-associated protein (MAp44) in regulating key components that influence the migration of cardiac neural crest cells, which is essential for heart development.
  • * Experiments in zebrafish models showed that knocking down MAp44 led to heart development issues and irregular heart functioning, but these problems could be reversed by restoring MAp44 levels, indicating the importance of immune molecules in heart tissue development.
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  • The complement system is a key part of the innate immune system, important for fighting infections and triggering inflammation.
  • The classical pathway of complement activation involves the C1 complex, composed of C1q and the protease complex C1rs, which binds to specific immune complexes (like those containing IgG or IgM).
  • New research reveals that the activation of C1 does not occur through intramolecular mechanisms as previously thought, but rather through interactions between neighboring C1 complexes, allowing for activation by a diverse range of molecular patterns.
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Since the discovery of the lectin pathway of complement activation, numerous clinical cohorts have been examined for one or more proteins, with the intention of uncovering the functions of the proteins or with the aim of discovering new biomarkers or diagnostic tools. To unveil the abnormal, it is pivotal to know the normal. Our aim was to describe the concentrations of the 11 known proteins of the lectin pathway in serum and plasma and to uncover possible gender differences, age and diurnal variations, which must be taken into account for investigation in different cohorts.

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Infiltrating activated monocytes are important mediators of damaging inflammation during influenza A virus (IAV) infection. We show that soluble respiratory proteins [collectins, surfactant proteins D (SP-D) and mannose binding lectin (MBL), H-ficolin and LL-37] inhibit replication of seasonal IAV in human monocytes. The collectins and H-ficolin also increased viral uptake by the cells, while LL-37 did not.

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The complement system is a part of the innate immune system and is involved in recognition and clearance of pathogens and altered-self structures. The lectin pathway of the complement system is initiated when soluble pattern recognition molecules (PRMs) with collagen-like regions bind to foreign or altered self-surfaces. Associated with the collagen-like stems of these PRMs are three mannan-binding lectin (MBL)-associated serine proteases (MASPs) and two MBL-associated proteins (MAps).

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  • * A study of 87 neonates with sepsis compared to controls found a higher frequency of low MBL genotypes in sepsis patients, but no notable differences in other lectin pathway or TLR receptor genes.
  • * The findings indicate low serum MBL and ficolin-2 levels are associated with sepsis, while alterations in protein concentrations rather than inherited genetic factors may reflect the disease's progression.
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  • - The study investigates the relationship between mannan-binding-lectin (MBL) deficiency, MAp44 levels, and outcomes in comatose survivors of out-of-hospital cardiac arrest (OHCA), postulating that MBL deficiency could lead to better outcomes.
  • - Researchers analyzed data from 169 patients, measuring MBL and MAp44 levels at various time points post-arrest, focusing on 30-day mortality and neurological outcomes at 180 days.
  • - The findings reveal no significant difference in mortality or neurological outcomes between patients with MBL deficiency and those with sufficient levels, indicating that neither factor correlates with patient recovery post-cardiac arrest.
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The objective of this study was to explore the involvement of collectin liver 1 (CL-L1) and collectin kidney 1 (CL-K1) and other pattern recognition molecules (PRMs) of the lectin pathway of the complement system in a cross-sectional cohort of systemic lupus erythematosus (SLE) patients. Concentrations in plasma of CL-L1, CL-K1, mannan-binding lectin (MBL), M-ficolin, H-ficolin and L-ficolin were determined in 58 patients with SLE and 65 healthy controls using time-resolved immunoflourometric assays. The SLE patients' demographic, diagnostic, clinical and biochemical data and collection of plasma samples were performed prospectively during 4 months.

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