C3 ‐dependent effector functions of complement

C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H 2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 ex...

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Published in:Immunological reviews Vol. 313; no. 1; pp. 120 - 138
Main Authors: Zarantonello, Alessandra, Revel, Margot, Grunenwald, Anne, Roumenina, Lubka T.
Format: Journal Article
Language:English
Published: England Wiley Subscription Services, Inc 01.01.2023
Wiley
John Wiley and Sons Inc
Subjects:
Anaphylatoxins
Binding Sites
Biochemistry, Molecular Biology
Biological activity
Cancer
Cell activation
Complement
Complement Activation
Complement C3 - analysis
Complement C3 - metabolism
Complement C3b - metabolism
Complement component C3
Complement component C3b
Complement component C3d
Complement receptors
Fragments
Humans
Immunology
Innate immunity
Invited Review
Invited Reviews
Life Sciences
Molecular structure
Opsonins
Receptors
Receptors, Complement - analysis
Structural Biology
cancer
autoimmunity
inflammation
anaphylatoxin
opsonin
complement C3
ISSN:0105-2896, 1600-065X, 1600-065X
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Abstract C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H 2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up‐to‐date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
AbstractList C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H 2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up‐to‐date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up-to-date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up-to-date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up-to-date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H₂O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up‐to‐date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H2O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up‐to‐date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding receptors. We will introduce the C3 forms (native C3, C3 [H2 O], and intracellular C3), the C3 fragments C3a, C3b, iC3b, and C3dg/C3d, and the C3 expression sites. To highlight the important role that C3 plays in human biological processes, we will give an overview of the diseases linked to C3 deficiency and to uncontrolled C3 activation. Next, we will present a structural description of C3 activation and of the C3 fragments generated by complement regulation. We will proceed by describing the C3a interaction with the anaphylatoxin receptor, followed by the interactions of opsonins (C3b, iC3b, and C3dg/C3d) with complement receptors, divided into two groups: receptors bearing complement regulatory functions and the effector receptors without complement regulatory activity. We outline the molecular architecture of the receptors, their binding sites on the C3 activation fragments, the cells expressing them, the diversity of their functions, and recent advances. With this review, we aim to give an up-to-date analysis of the processes triggered by C3 activation fragments on different cell types in health and disease contexts.
Author Roumenina, Lubka T.
Revel, Margot
Grunenwald, Anne
Zarantonello, Alessandra
AuthorAffiliation 1 Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
AuthorAffiliation_xml – name: 1 Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
Author_xml – sequence: 1
  givenname: Alessandra
  surname: Zarantonello
  fullname: Zarantonello, Alessandra
  organization: Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
– sequence: 2
  givenname: Margot
  surname: Revel
  fullname: Revel, Margot
  organization: Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
– sequence: 3
  givenname: Anne
  surname: Grunenwald
  fullname: Grunenwald, Anne
  organization: Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
– sequence: 4
  givenname: Lubka T.
  orcidid: 0000-0002-9940-0324
  surname: Roumenina
  fullname: Roumenina, Lubka T.
  organization: Centre de Recherche des Cordeliers INSERM, Sorbonne Université, Université de Paris Paris France
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36271889$$D View this record in MEDLINE/PubMed
https://hal.sorbonne-universite.fr/hal-03829321$$DView record in HAL
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Issue 1
Keywords cancer
autoimmunity
inflammation
anaphylatoxin
opsonin
complement C3
Language English
License 2022 The Authors. Immunological Reviews published by John Wiley & Sons Ltd.
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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This article is part of a series of reviews covering The Alternative Pathway or Amplification Loop of Complement appearing in Volume 313 of Immunological Reviews.
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Snippet C3 is the central effector molecule of the complement system, mediating its multiple functions through different binding sites and their corresponding...
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StartPage 120
SubjectTerms Anaphylatoxins
Binding Sites
Biochemistry, Molecular Biology
Biological activity
Cancer
Cell activation
Complement
Complement Activation
Complement C3 - analysis
Complement C3 - metabolism
Complement C3b - metabolism
Complement component C3
Complement component C3b
Complement component C3d
Complement receptors
Fragments
Humans
Immunology
Innate immunity
Invited Review
Invited Reviews
Life Sciences
Molecular structure
Opsonins
Receptors
Receptors, Complement - analysis
Structural Biology
Title C3 ‐dependent effector functions of complement
URI https://www.ncbi.nlm.nih.gov/pubmed/36271889
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https://pubmed.ncbi.nlm.nih.gov/PMC10092904
Volume 313
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