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Masaru Nonaka - One of the best experts on this subject based on the ideXlab platform.

  • Primitive Complement System--recognition and activation.
    Molecular immunology, 2020
    Co-Authors: Teizo Fujita, Yuichi Endo, Masaru Nonaka
    Abstract:

    The Complement System, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are one of the pattern recognition molecules acting in innate immunity and upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-base Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and functions in an opsonic manner. On the other hand, ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian Complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian Complement components are present only in deuterostomes, indicating the deuterostome origin of the Complement System. Unexpectedly, the Complement System of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals, suggesting that expansion of Complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian Complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity in several points. Thus, another integrative step seems to have been required to establish the modern Complement System of higher vertebrates.

  • Origin and evolution of the Complement System.
    Current Topics in Microbiology and Immunology, 2020
    Co-Authors: Masaru Nonaka
    Abstract:

    The vertebrate immune System is composed of two parts, innate immunity which recognizes the invading microbes using germline-encoded molecules, and adaptive immunity, which depends on recognition molecules generated by somatic mechanisms during the ontogeny of each individual organism (Medzhitov and Janeway 1997). All data available to date indicate that adaptive immunity became established at the early stage of vertebrate evolution around the time of cartilaginous fish emergence. Thus the genes which encode the pivotal elements of adaptive immunity, such as immunoglobulin (Litman et al. 1993), T-cell receptor (Rast et al. 1997), major histocompatibility complex (MHC) class I (Hasulmoto et al. 1992) and class II molecules (Kasahara et al. 1992; Bartle and Weissman 1994) and recombination activating gene (Greenhalgh and Steiner 1995) have been identified in cartilaginous fish and higher vertebrates. None of the attempts to isolate these genes from the most primitive extant vertebrates, cyclostomes, has yet succeeded. In contrast, vertebrate innate immunity is believed to have a more ancient origin, and an apparently primitive Complement System has been found in lamprey (Nonaka et al. 1983). However, it was not clear until recently whether the origin of the Complement System can be traced back to invertebrate. Identification of C3/C4/C5-like expressed sequence tag (Est) from sea urchin coelomocytes (Smith et al. 1996) and molecular studies of the Complement System in sea urchin and ascidian established the presence of the multicomponent, opsonic Complement System in invertebrates.

  • evolution of the Complement System
    Sub-cellular biochemistry, 2014
    Co-Authors: Masaru Nonaka
    Abstract:

    : The mammalian Complement System constitutes a highly sophisticated body defense machinery comprising more than 30 components. Research into the evolutionary origin of the Complement System has identified a primitive version composed of the central component C3 and two activation proteases Bf and MASP in cnidaria. This suggests that the Complement System was established in the common ancestor of eumetazoa more than 500 million years ago. The original activation mechanism of the original Complement System is believed to be close to the mammalian lectin and alternative activation pathways, and its main role seems to be opsonization and induction of inflammation. This primitive Complement System has been retained by most deuterostomes without major change until the appearance of jawed vertebrates. At this stage, duplication of the C3, Bf and MASP genes as well as recruitment of membrane attack components added the classical and lytic pathways to the primitive Complement System, converting it to the modern Complement System. In contrast, the Complement System was lost multiple times independently in the protostome lineage.

  • eLS - Complement System: Evolution
    eLS, 2013
    Co-Authors: Masaru Nonaka
    Abstract:

    The human Complement System is one of the principal effector Systems of innate immunity and consists of more than 30 serum and cell surface proteins. Most Complement components show a striking modular structure, which makes evolutionary studies feasible. The evolutionary origin of the Complement System can be traced back to the common ancestor of eumetazoa, predating by far the origin of the canonical adaptive immunity unique to the jawed vertebrates. Although the Complement System has been conserved by all deuterostomes analysed thus far, it has been lost multiple times independently in the protostome lineage. Sophistication of the Complement System from a simpler System by gene duplications and exon shuffling occurred in the vertebrate lineage. Key Concepts: The Complement System is one of the most ancient body defence mechanisms of eumetazoa. Most Complement components have a characteristic modular structure. The modern Complement System was established in a common ancestor of jawed vertebrates by gene duplication and exon shuffling of the primitive Complement genes. The Complement System has been lost multiple times independently in protostome lineages, whereas it has been retained by all deuterostomes analysed so far. The thioester-containing protein family is subdivided into two subfamilies, the C3 and A2M subfamilies. Keywords: gene duplication; modular structure; innate immunity; deuterostome; protostome; cnidaria

  • Genomic view of the evolution of the Complement System
    Immunogenetics, 2006
    Co-Authors: Masaru Nonaka, Ayuko Kimura
    Abstract:

    The recent accumulation of genomic information of many representative animals has made it possible to trace the evolution of the Complement System based on the presence or absence of each Complement gene in the analyzed genomes. Genome information from a few mammals, chicken, clawed frog, a few bony fish, sea squirt, fruit fly, nematoda and sea anemone indicate that bony fish and higher vertebrates share practically the same set of Complement genes. This suggests that most of the gene duplications that played an essential role in establishing the mammalian Complement System had occurred by the time of the teleost/mammalian divergence around 500 million years ago (MYA). Members of most Complement gene families are also present in ascidians, although they do not show a one-to-one correspondence to their counterparts in higher vertebrates, indicating that the gene duplications of each gene family occurred independently in vertebrates and ascidians. The C3 and factor B genes, but probably not the other Complement genes, are present in the genome of the cnidaria and some protostomes, indicating that the origin of the central part of the Complement System was established more than 1,000 MYA.

Teizo Fujita - One of the best experts on this subject based on the ideXlab platform.

  • Primitive Complement System--recognition and activation.
    Molecular immunology, 2020
    Co-Authors: Teizo Fujita, Yuichi Endo, Masaru Nonaka
    Abstract:

    The Complement System, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are one of the pattern recognition molecules acting in innate immunity and upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-base Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and functions in an opsonic manner. On the other hand, ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian Complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian Complement components are present only in deuterostomes, indicating the deuterostome origin of the Complement System. Unexpectedly, the Complement System of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals, suggesting that expansion of Complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian Complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity in several points. Thus, another integrative step seems to have been required to establish the modern Complement System of higher vertebrates.

  • lectin Complement System and pattern recognition
    Immunobiology, 2006
    Co-Authors: Yuichi Endo, M Takahashi, Teizo Fujita
    Abstract:

    Abstract Living organisms have strong defense mechanisms against invading microorganisms as survival strategies. One of the defense mechanisms is the Complement System, composed of more than 30 serum and cell surface components. This System collaborates in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are pattern recognition proteins acting in innate immunity and, upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-based Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and in lamprey, the most primitive vertebrate. Furthermore, a lamprey N -acetylglucosamine (GlcNAc)-binding lectin was identified as the orthlogue of mammalian C1q, and lamprey MASP is suggested as the prototype of MASP-2/C1r/C1s, indicating that the classical Complement pathway arose as a part of the innate immune System. Thus, the Complement System is one of the most highly organized innate immune Systems in invertebrates and jawless vertebrates, and this System has survived in vertebrates with its core components little changed for 600–700 million years.

  • Primitive Complement System--recognition and activation.
    Molecular Immunology, 2004
    Co-Authors: Teizo Fujita, Yuichi Endo, Masaru Nonaka
    Abstract:

    The Complement System, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are one of the pattern recognition molecules acting in innate immunity and upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-base Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and functions in an opsonic manner. On the other hand, ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian Complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian Complement components are present only in deuterostomes, indicating the deuterostome origin of the Complement System. Unexpectedly, the Complement System of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals, suggesting that expansion of Complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian Complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity in several points. Thus, another integrative step seems to have been required to establish the modern Complement System of higher vertebrates. © 2004 Elsevier Ltd. All rights reserved.

Yuichi Endo - One of the best experts on this subject based on the ideXlab platform.

  • Primitive Complement System--recognition and activation.
    Molecular immunology, 2020
    Co-Authors: Teizo Fujita, Yuichi Endo, Masaru Nonaka
    Abstract:

    The Complement System, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are one of the pattern recognition molecules acting in innate immunity and upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-base Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and functions in an opsonic manner. On the other hand, ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian Complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian Complement components are present only in deuterostomes, indicating the deuterostome origin of the Complement System. Unexpectedly, the Complement System of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals, suggesting that expansion of Complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian Complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity in several points. Thus, another integrative step seems to have been required to establish the modern Complement System of higher vertebrates.

  • lectin Complement System and pattern recognition
    Immunobiology, 2006
    Co-Authors: Yuichi Endo, M Takahashi, Teizo Fujita
    Abstract:

    Abstract Living organisms have strong defense mechanisms against invading microorganisms as survival strategies. One of the defense mechanisms is the Complement System, composed of more than 30 serum and cell surface components. This System collaborates in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are pattern recognition proteins acting in innate immunity and, upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-based Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and in lamprey, the most primitive vertebrate. Furthermore, a lamprey N -acetylglucosamine (GlcNAc)-binding lectin was identified as the orthlogue of mammalian C1q, and lamprey MASP is suggested as the prototype of MASP-2/C1r/C1s, indicating that the classical Complement pathway arose as a part of the innate immune System. Thus, the Complement System is one of the most highly organized innate immune Systems in invertebrates and jawless vertebrates, and this System has survived in vertebrates with its core components little changed for 600–700 million years.

  • Primitive Complement System--recognition and activation.
    Molecular Immunology, 2004
    Co-Authors: Teizo Fujita, Yuichi Endo, Masaru Nonaka
    Abstract:

    The Complement System, composed of more than 30 serum and cell surface components, is collaborating in recognition and elimination of pathogens as a part of both the innate and acquired immune Systems. The two collagenous lectins, mannose-binding lectin (MBL) and ficolins, are one of the pattern recognition molecules acting in innate immunity and upon recognition of the pathogens, they trigger the activation of the lectin Complement pathway through attached serine proteases (MASPs). A similar lectin-base Complement System, consisting of the lectin-protease complex and C3, is present in ascidians, our closest invertebrate relatives and functions in an opsonic manner. On the other hand, ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian Complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian Complement components are present only in deuterostomes, indicating the deuterostome origin of the Complement System. Unexpectedly, the Complement System of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals, suggesting that expansion of Complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian Complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity in several points. Thus, another integrative step seems to have been required to establish the modern Complement System of higher vertebrates. © 2004 Elsevier Ltd. All rights reserved.

Jean F Regal - One of the best experts on this subject based on the ideXlab platform.

  • the Complement System and preeclampsia
    Current Hypertension Reports, 2017
    Co-Authors: Jean F Regal, Richard M Burwick, Sherry D Fleming
    Abstract:

    Purpose of Review Preeclampsia affects 3–4% of pregnancies with few treatment options to reduce maternal and fetal harm. Recent evidence that targeting the Complement System may be an effective therapeutic strategy in prevention or treatment of preeclampsia will be reviewed.

  • the Complement System and adverse pregnancy outcomes
    Molecular Immunology, 2015
    Co-Authors: Jean F Regal, Jeffrey S Gilbert, Richard M Burwick
    Abstract:

    Abstract Adverse pregnancy outcomes significantly contribute to morbidity and mortality for mother and child, with lifelong health consequences for both. The innate and adaptive immune System must be regulated to insure survival of the fetal allograft, and the Complement System is no exception. An intact Complement System optimizes placental development and function and is essential to maintain host defense and fetal survival. Complement regulation is apparent at the placental interface from early pregnancy with some degree of Complement activation occurring normally throughout gestation. However, a number of pregnancy complications including early pregnancy loss, fetal growth restriction, hypertensive disorders of pregnancy and preterm birth are associated with excessive or misdirected Complement activation, and are more frequent in women with inherited or acquired Complement System disorders or Complement gene mutations. Clinical studies employing Complement biomarkers in plasma and urine implicate dysregulated Complement activation in components of each of the adverse pregnancy outcomes. In addition, mechanistic studies in rat and mouse models of adverse pregnancy outcomes address the Complement pathways or activation products of importance and allow critical analysis of the pathophysiology. Targeted Complement therapeutics are already in use to control adverse pregnancy outcomes in select situations. A clearer understanding of the role of the Complement System in both normal pregnancy and complicated or failed pregnancy will allow a rational approach to future therapeutic strategies for manipulating Complement with the goal of mitigating adverse pregnancy outcomes, preserving host defense, and improving long term outcomes for both mother and child.

Richard M Burwick - One of the best experts on this subject based on the ideXlab platform.

  • the Complement System and preeclampsia
    Current Hypertension Reports, 2017
    Co-Authors: Jean F Regal, Richard M Burwick, Sherry D Fleming
    Abstract:

    Purpose of Review Preeclampsia affects 3–4% of pregnancies with few treatment options to reduce maternal and fetal harm. Recent evidence that targeting the Complement System may be an effective therapeutic strategy in prevention or treatment of preeclampsia will be reviewed.

  • the Complement System and adverse pregnancy outcomes
    Molecular Immunology, 2015
    Co-Authors: Jean F Regal, Jeffrey S Gilbert, Richard M Burwick
    Abstract:

    Abstract Adverse pregnancy outcomes significantly contribute to morbidity and mortality for mother and child, with lifelong health consequences for both. The innate and adaptive immune System must be regulated to insure survival of the fetal allograft, and the Complement System is no exception. An intact Complement System optimizes placental development and function and is essential to maintain host defense and fetal survival. Complement regulation is apparent at the placental interface from early pregnancy with some degree of Complement activation occurring normally throughout gestation. However, a number of pregnancy complications including early pregnancy loss, fetal growth restriction, hypertensive disorders of pregnancy and preterm birth are associated with excessive or misdirected Complement activation, and are more frequent in women with inherited or acquired Complement System disorders or Complement gene mutations. Clinical studies employing Complement biomarkers in plasma and urine implicate dysregulated Complement activation in components of each of the adverse pregnancy outcomes. In addition, mechanistic studies in rat and mouse models of adverse pregnancy outcomes address the Complement pathways or activation products of importance and allow critical analysis of the pathophysiology. Targeted Complement therapeutics are already in use to control adverse pregnancy outcomes in select situations. A clearer understanding of the role of the Complement System in both normal pregnancy and complicated or failed pregnancy will allow a rational approach to future therapeutic strategies for manipulating Complement with the goal of mitigating adverse pregnancy outcomes, preserving host defense, and improving long term outcomes for both mother and child.