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<title>Classical complement pathway</title>

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<span id="openzim-page-title" class="mw-page-title-main"><span class="mw-page-title-main">Classical complement pathway</span></span>

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<p>The <b>classical complement pathway</b> is one of three pathways which activate the <a href="Complement_system" title="Complement system">complement system</a>, which is part of the <a href="Immune_system" title="Immune system">immune system</a>. The classical complement pathway is initiated by <a href="Antigen-antibody_complex" class="mw-redirect" title="Antigen-antibody complex">antigen-antibody complexes</a> with the antibody isotypes <a href="Immunoglobulin_G" title="Immunoglobulin G">IgG</a> and <a href="Immunoglobulin_M" title="Immunoglobulin M">IgM</a>.<sup id="cite_ref-Overview_of_Complement_1-0" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Complement_in_disease_2-0" class="reference"><a href="#cite_note-Complement_in_disease-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup>

</p><p>Following activation, a series of <a href="Protein" title="Protein">proteins</a> are recruited to generate <a href="C3-convertase" title="C3-convertase">C3 convertase</a> (C4b2b, <a href="Complement_system#Complement_protein_fragment_nomenclature" title="Complement system">historically</a> referred C4b2a), which cleaves the <a href="Complement_component_3" title="Complement component 3">C3</a> protein. The <a href="C3b" title="C3b">C3b</a> component of the cleaved C3 binds to C3 convertase (C4b2b) to generate <a href="C5-convertase" title="C5-convertase">C5 convertase</a> (C4b2b3b), which cleaves the <a href="Complement_component_5" title="Complement component 5">C5</a> protein. The cleaved products attract phagocytes to the site of infection and tags target cells for elimination by phagocytosis. In addition, the C5 convertase initiates the terminal phase of the complement system, leading to the assembly of the membrane attack complex (<a href="Complement_membrane_attack_complex" title="Complement membrane attack complex">MAC</a>). The membrane attack complex creates a pore on the target cell's membrane, inducing cell lysis and death.<sup id="cite_ref-Complement_in_disease_2-1" class="reference"><a href="#cite_note-Complement_in_disease-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Complement_history_3-0" class="reference"><a href="#cite_note-Complement_history-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup>

</p><p>The classical complement pathway can also be activated by <a href="Apoptotic" class="mw-redirect" title="Apoptotic">apoptotic</a> cells, necrotic cells, and <a href="Acute_phase_protein" class="mw-redirect" title="Acute phase protein">acute phase proteins</a>.<sup id="cite_ref-Overview_of_Complement_1-1" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Complement_history_3-1" class="reference"><a href="#cite_note-Complement_history-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-C1q_4-0" class="reference"><a href="#cite_note-C1q-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup>

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<div class="mw-heading mw-heading2"><h2 id="Complement_cascade">Complement cascade</h2></div>

<p>The classical pathway is distinct from the other complement pathways in its unique activation triggers and cascade sequence. Activation of the complement pathway through the classical, <a href="Lectin_pathway" title="Lectin pathway">lectin</a> or <a href="Alternative_complement_pathway" title="Alternative complement pathway">alternative complement pathway</a> is followed by a cascade of reactions eventually leading to the membrane attack complex.

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<div class="mw-heading mw-heading3"><h3 id="Initiation">Initiation</h3></div>

<p>The classical complement pathway can be initiated by the binding of antigen-antibody complexes to the <a href="Complement_component_1q" title="Complement component 1q">C1q</a> protein. The globular regions of C1q recognize and bind to the <a href="Fragment_crystallizable_region" title="Fragment crystallizable region">Fc</a> region of antibody isotypes IgG or IgM.<sup id="cite_ref-Complement_in_disease_2-2" class="reference"><a href="#cite_note-Complement_in_disease-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup> These globular regions of C1q can also bind to bacterial and viral surface proteins, apoptotic cells, and acute phase proteins.<sup id="cite_ref-5" class="reference"><a href="#cite_note-5"><span class="cite-bracket">[</span>5<span class="cite-bracket">]</span></a></sup> In the absence of these activation factors, C1q is part of the inactive C1 complex which consists of six molecules of C1q, two molecules of <a href="C1r" class="mw-redirect" title="C1r">C1r</a>, and two molecules of <a href="C1s" class="mw-redirect" title="C1s">C1s</a>.<sup id="cite_ref-Overview_of_Complement_1-2" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-C1q_4-1" class="reference"><a href="#cite_note-C1q-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup>

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<div class="mw-heading mw-heading3"><h3 id="Formation_of_C4b_convertase">Formation of C4b convertase</h3></div>

<p>The binding of C1q with pathogen surface or antigen-antibody immune complex leads to conformational changes and the activation of the serine protease C1r. The activated C1r then cleaves and activates the serine protease C1s.<sup id="cite_ref-Complement_history_3-2" class="reference"><a href="#cite_note-Complement_history-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-C1q_4-2" class="reference"><a href="#cite_note-C1q-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup> Activated C1s cleaves <a href="Complement_component_4" title="Complement component 4">C4</a> into C4a and C4b.

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<div class="mw-heading mw-heading3"><h3 id="Regulation_of_C4b">Regulation of C4b</h3></div>

<p>The newly formed C4b cannot stay activated as a highly reactive thioester bond is revealed once C4 has been cleaved. The thioester bond is cleaved by water resulting in its cleavage permanently deactivating the C4b molecule. As a result of this C4b is restricted to only bind to pathogen surfaces. They would undergo rapid deactivation in the time it took to travel from the origin of activation where C1q is complexed with an antigen-antibody immune complex(IC) or where C1q is directly attached to the pathogens surface.<sup id="cite_ref-:1_6-0" class="reference"><a href="#cite_note-:1-6"><span class="cite-bracket">[</span>6<span class="cite-bracket">]</span></a></sup>

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<div class="mw-heading mw-heading3"><h3 id="Formation_of_C3-convertase.">Formation of C3-convertase.</h3></div>

<p>Surface-bound C4b acts as a receptor for the binding of C2.<sup id="cite_ref-:1_6-1" class="reference"><a href="#cite_note-:1-6"><span class="cite-bracket">[</span>6<span class="cite-bracket">]</span></a></sup> The binding of C2 and C4b results in C2 being cleaved by C1s into C2a and C2b. C2b diffuses into the plasma as a protein inflammatory mediator while C2a remains attached with C4b, forming the C3-convertase (C4b2a). The function of the membrane-bound C3-convertase is the cleavage of many many molecules of C3 into C3a and C3b. C3a is a smaller fragment of C3 is a potent inflammatory mediator.

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<div class="mw-heading mw-heading3"><h3 id="C3b_function_and_structure.">C3b function and structure.</h3></div>

<p>C3b can act as an opsonin. C3b is very similar to C4 in both structure and function also has a thioester bond that forces it to attach to surface nucleophile of the activator(namely the pathogen or IC). Phagocytes have receptors for C3b and as a result of receptor-ligand binding are able to more easily recognize and engulf pathogen molecules. While the <a href="Anaphylatoxin" title="Anaphylatoxin">anaphylatoxin</a> C3a interacts with its <a href="C3a_receptor" title="C3a receptor">C3a receptor</a> (C3aR) to recruit leukocytes, C3b contributes to further downstream complement activation.<sup id="cite_ref-Overview_of_Complement_1-3" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Complement_history_3-3" class="reference"><a href="#cite_note-Complement_history-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup>

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<div class="mw-heading mw-heading3"><h3 id="Formation_of_C5_convertase_and_MAC">Formation of C5 convertase and MAC</h3></div>

<p>C3b binds to the C3 convertase (C4b2a), to form C5 convertase (C4b2a3b). C5 convertase then cleaves C5 into C5a and C5b.<sup id="cite_ref-Complement_history_3-4" class="reference"><a href="#cite_note-Complement_history-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup> Like C3a, C5a is also an anaphylatoxin that interacts with its cognate C5a receptor (C5aR) to attract leukocytes.<sup id="cite_ref-Overview_of_Complement_1-4" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup> Subsequent interactions between C5b and other terminal components C6, C7, C8, and C9 form the membrane attack complex or the C5b-9 complex which forms pores on the target cell membranes to lysing.<sup id="cite_ref-Rus_103–112_7-0" class="reference"><a href="#cite_note-Rus_103–112-7"><span class="cite-bracket">[</span>7<span class="cite-bracket">]</span></a></sup>

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<div class="mw-heading mw-heading2"><h2 id="Clinical_significance">Clinical significance</h2></div>

<p>Because of its role in the innate immune system classical complement has been implicated in a number of pathogen related disorders. Complement is responsible for immune inflammatory response in adipose tissues which has been implicated in the development of <a href="Obesity" title="Obesity">obesity</a>.<sup id="cite_ref-:0_8-0" class="reference"><a href="#cite_note-:0-8"><span class="cite-bracket">[</span>8<span class="cite-bracket">]</span></a></sup> Obesity in turn results in an abnormally high level of complement activation via production of the C1 component of the classical pathway, which can lead to tissue inflammation and eventually <a href="Insulin_resistance" title="Insulin resistance">insulin resistance</a>, however the exact mechanisms that causes this is yet unknown.<sup id="cite_ref-:0_8-1" class="reference"><a href="#cite_note-:0-8"><span class="cite-bracket">[</span>8<span class="cite-bracket">]</span></a></sup>

</p><p>Immunotherapies have been developed to detect and destroy cells infected by the HIV virus via classical complement activation.<sup id="cite_ref-9" class="reference"><a href="#cite_note-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> This process involves creating synthetic peptides that target conserved regions in HIV specific proteins and induce an antibody specific immune response through IgG antibodies. This is important for targeting the virus in its intracellular phase because the antibodies specific to the synthetic peptides can trigger the classical complement pathway and induce the death of HIV infected cells.

</p><p>Classical complement activation has also been shown to combat Methicillin-resistant Staphylococcus aureus.<sup id="cite_ref-10" class="reference"><a href="#cite_note-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> Certain variants of the IgM antibody were found to bind the Methicillin-resistant <i><a href="Staphylococcus_aureus" title="Staphylococcus aureus">Staphylococcus aureus</a></i> these IgM were found to be critical in complement activation through the classical pathway and subsequent destruction of the bacteria. Therapies that utilize classical complement activation have been shown to be effective in targeting and killing cancer cells and destroying tumors.<sup id="cite_ref-11" class="reference"><a href="#cite_note-11"><span class="cite-bracket">[</span>11<span class="cite-bracket">]</span></a></sup> <a href="Tachyplesin" title="Tachyplesin">Tachyplesin</a>, a small peptide, has been shown to exhibit these effects. When injected into target tissue encourages recruitment of C1q and activates downstream events, eventually leading to the formation of the C5b-9 complex which damages tumor cells, killing them.

</p><p>Lack of regulation of the classical complement pathway through the deficiency in <a href="C1-inhibitor" title="C1-inhibitor">C1-inhibitor</a> results in episodic <a href="Angioedema" title="Angioedema">angioedema</a>.<sup id="cite_ref-Overview_of_Complement_1-5" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup> C1-inhibitor defiency can be hereditary or acquired, resulting in hereditary or acquired angioedema.<sup id="cite_ref-angiodema_12-0" class="reference"><a href="#cite_note-angiodema-12"><span class="cite-bracket">[</span>12<span class="cite-bracket">]</span></a></sup> C1-inhibitor plays the role of inactivating C1r and C1s to prevent further downstream classical complement activity.<sup id="cite_ref-13" class="reference"><a href="#cite_note-13"><span class="cite-bracket">[</span>13<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-angiodema_12-1" class="reference"><a href="#cite_note-angiodema-12"><span class="cite-bracket">[</span>12<span class="cite-bracket">]</span></a></sup> C1-inhibitor controls the processes involved in maintaining vascular permeability. As a result, C1-inhibitor levels of less than 50% of the standard lead to increased vascular permeability, characteristic of angioedema.<sup id="cite_ref-angiodema_12-2" class="reference"><a href="#cite_note-angiodema-12"><span class="cite-bracket">[</span>12<span class="cite-bracket">]</span></a></sup> Cinryze, a human plasma derived C1-esterase inhibitor, has been approved for use in 2008 for the prevention of hereditary angioedema attacks.<sup id="cite_ref-14" class="reference"><a href="#cite_note-14"><span class="cite-bracket">[</span>14<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-15" class="reference"><a href="#cite_note-15"><span class="cite-bracket">[</span>15<span class="cite-bracket">]</span></a></sup>

</p><p>Deficiency in the <a href="Complement_component_1q" title="Complement component 1q">C1q</a> protein of the classical complement pathway can lead to development of <a href="Systemic_lupus_erythematosus" class="mw-redirect" title="Systemic lupus erythematosus">systemic lupus erythematosus</a>.<sup id="cite_ref-Complement_in_disease_2-3" class="reference"><a href="#cite_note-Complement_in_disease-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-16" class="reference"><a href="#cite_note-16"><span class="cite-bracket">[</span>16<span class="cite-bracket">]</span></a></sup> Among the many functions of C1q, C1q triggers clearance of immune complexes and apoptotic cells by activating the classical pathway and binding directly onto phagocytes.<sup id="cite_ref-Overview_of_Complement_1-6" class="reference"><a href="#cite_note-Overview_of_Complement-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-17" class="reference"><a href="#cite_note-17"><span class="cite-bracket">[</span>17<span class="cite-bracket">]</span></a></sup> Consequently, systemic lupus erythematosus from insufficient amounts of C1q is characterized by the accumulation of autoantibodies and apoptotic cells.<sup id="cite_ref-C1q_4-3" class="reference"><a href="#cite_note-C1q-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup> Studies are being done to look into antibodies against C1q as a diagnostic marker for systemic lupus erythematosus.<sup id="cite_ref-18" class="reference"><a href="#cite_note-18"><span class="cite-bracket">[</span>18<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-19" class="reference"><a href="#cite_note-19"><span class="cite-bracket">[</span>19<span class="cite-bracket">]</span></a></sup>

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<ul><li><a href="Alternative_complement_pathway" title="Alternative complement pathway">Alternative complement pathway</a></li>

<li><a href="Lectin_pathway" title="Lectin pathway">Lectin pathway</a></li></ul>

<div class="mw-heading mw-heading2"><h2 id="References">References</h2></div>

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</ol></div></div>

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</style><div id="Lymphocytic_adaptive_immune_system_and_complement123" style="font-size:114%;margin:0 4em"><a href="Lymphocyte" title="Lymphocyte">Lymphocytic</a> <a href="Adaptive_immune_system" title="Adaptive immune system">adaptive immune system</a> and <a href="Complement_system" title="Complement system">complement</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%">Lymphoid</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Antigens</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Antigen" title="Antigen">Antigen</a>

<ul><li><a href="Superantigen" title="Superantigen">Superantigen</a></li>

<li><a href="Allergen" title="Allergen">Allergen</a></li>

<li><a href="Antigenic_variation" title="Antigenic variation">Antigenic variation</a></li></ul></li>

<li><a href="Hapten" title="Hapten">Hapten</a></li></ul>

<ul><li><a href="Epitope" title="Epitope">Epitope</a>

<ul><li><a href="Linear_epitope" title="Linear epitope">Linear</a></li>

<li><a href="Conformational_epitope" title="Conformational epitope">Conformational</a></li></ul></li>

<li><a href="Mimotope" title="Mimotope">Mimotope</a></li></ul>

<ul><li><a href="Antigen_presentation" title="Antigen presentation">Antigen presentation</a>/<a href="Antigen-presenting_cell" title="Antigen-presenting cell">professional APCs</a>: <a href="Dendritic_cell" title="Dendritic cell">Dendritic cell</a></li>

<li><a href="Macrophage" title="Macrophage">Macrophage</a></li>

<li><a href="Immunogen" title="Immunogen">Immunogen</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Antibodies</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Antibody" title="Antibody">Antibody</a>

<ul><li><a href="Monoclonal_antibody" title="Monoclonal antibody">Monoclonal antibodies</a></li>

<li><a href="Polyclonal_antibodies" title="Polyclonal antibodies">Polyclonal antibodies</a></li>

<li><a href="Autoantibody" title="Autoantibody">Autoantibody</a></li>

<li><a href="Microantibody" title="Microantibody">Microantibody</a></li></ul></li>

<li><a href="Polyclonal_B_cell_response" title="Polyclonal B cell response">Polyclonal B cell response</a></li>

<li><a href="Allotype_(immunology)" title="Allotype (immunology)">Allotype</a></li>

<li><a href="Isotype_(immunology)" title="Isotype (immunology)">Isotype</a></li>

<li><a href="Idiotype" title="Idiotype">Idiotype</a></li></ul>

<ul><li><a href="Immune_complex" title="Immune complex">Immune complex</a></li>

<li><a href="Paratope" title="Paratope">Paratope</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Immunity vs.<br> tolerance</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li>Action: <a href="Immunity_(medical)" class="mw-redirect" title="Immunity (medical)">Immunity</a></li>

<li><a href="Autoimmunity" title="Autoimmunity">Autoimmunity</a></li>

<li><a href="Alloimmunity" title="Alloimmunity">Alloimmunity</a></li>

<li><a href="Allergy" title="Allergy">Allergy</a></li>

<li><a href="Hypersensitivity" title="Hypersensitivity">Hypersensitivity</a></li>

<li><a href="Inflammation" title="Inflammation">Inflammation</a></li>

<li><a href="Cross-reactivity" title="Cross-reactivity">Cross-reactivity</a></li>

<li><a href="Co-stimulation" title="Co-stimulation">Co-stimulation</a></li></ul>

<ul><li>Inaction: <a href="Immune_tolerance" title="Immune tolerance">Tolerance</a>

<ul><li><a href="Central_tolerance" title="Central tolerance">Central</a></li>

<li><a href="Peripheral_tolerance" title="Peripheral tolerance">Peripheral</a></li>

<li><a href="Clonal_anergy" title="Clonal anergy">Clonal anergy</a></li>

<li><a href="Clonal_deletion" title="Clonal deletion">Clonal deletion</a></li>

<li><a href="T-cell_depletion" title="T-cell depletion">T-cell depletion</a></li>

<li><a href="Immune_tolerance_in_pregnancy" title="Immune tolerance in pregnancy">Tolerance in pregnancy</a></li></ul></li>

<li><a href="Immunodeficiency" title="Immunodeficiency">Immunodeficiency</a></li>

<li><a href="Immune_privilege" title="Immune privilege">Immune privilege</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="Immunogenetics" title="Immunogenetics">Immunogenetics</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Affinity_maturation" title="Affinity maturation">Affinity maturation</a>

<ul><li><a href="Somatic_hypermutation" title="Somatic hypermutation">Somatic hypermutation</a></li>

<li><a href="Clonal_selection" title="Clonal selection">Clonal selection</a></li></ul></li>

<li><a href="V(D)J_recombination" title="V(D)J recombination">V(D)J recombination</a></li>

<li><a href="Junctional_diversity" title="Junctional diversity">Junctional diversity</a></li>

<li><a href="Immunoglobulin_class_switching" title="Immunoglobulin class switching">Immunoglobulin class switching</a></li>

</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="Lymphocyte" title="Lymphocyte">Lymphocytes</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Cell-mediated_immunity" title="Cell-mediated immunity">Cellular</a>

<li><a href="Humoral_immunity" title="Humoral immunity">Humoral</a>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Substances</th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Cytokine" title="Cytokine">Cytokines</a></li>

<li><a href="Opsonin" title="Opsonin">Opsonin</a></li>

<li><a href="Cytolysin" title="Cytolysin">Cytolysin</a></li></ul>

</div></td></tr></tbody></table></div>

<div class="navbox-styles"></div><div role="navigation" class="navbox" aria-labelledby="Complement_system89" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2"><div id="Complement_system89" style="font-size:114%;margin:0 4em"><a href="Complement_system" title="Complement system">Complement system</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%">Pathways</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Activators/enzymes</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Early</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><i>A:</i> <a href="Complement_factor_B" title="Complement factor B">Factor B</a></li>

<li><a href="Factor_D" title="Factor D">Factor D</a></li>

<li><a href="Properdin" title="Properdin">Factor P/Properdin</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Middle</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="C3-convertase" title="C3-convertase">C3-convertase</a></li>

<li><a href="C5-convertase" title="C5-convertase">C5-convertase</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Late</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">

</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Inhibitors</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><i>CLA:</i> <a href="C1-inhibitor" title="C1-inhibitor">C1-inhibitor</a></li>

<li><a href="Decay-accelerating_factor" title="Decay-accelerating factor">Decay-accelerating factor</a>/<a href="CD59" title="CD59">CD59</a></li>

<li><a href="Complement_factor_I" title="Complement factor I">Factor I</a></li></ul>

<ul><li><i>A:</i> <a href="Factor_H" title="Factor H">Factor H</a></li></ul>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="Complement_receptor" title="Complement receptor">Complement receptors</a></th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<li><a href="Anaphylatoxin_receptors" title="Anaphylatoxin receptors">Anaphylatoxin</a>

</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Function</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">

<ul><li><a href="Cytotoxicity" title="Cytotoxicity">Cytotoxicity</a>(by MAC)</li>

<li><a href="Immune_adherence" title="Immune adherence">immune adherence</a></li>

<li>Inducing <a href="Inflammation" title="Inflammation">inflammation</a></li>

<li><a href="Opsonization" class="mw-redirect" title="Opsonization">Opsonization</a></li></ul>

</div></td></tr></tbody></table></div></div><div><div class="zim-footer">

This article is issued from <a class="external text" title="Last edited on 2025-05-29" href="https://en.wikipedia.org/wiki/?title=Classical_complement_pathway&oldid=1292954946">Wikipedia</a>. The text is available under <a class="external text" href="https://creativecommons.org/licenses/by-sa/4.0/deed.en">Creative Commons Attribution-Share Alike 4.0</a> unless otherwise noted. Additional terms may apply for the media files.

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