C3b

出典: meddic

補体

  • 古典的経路:C3からC4b2aのもつC3 convatase活性により生成し、C4b2a3bはC5 convertase活性を持つ (2008前期免疫学プリント 68)
  • 別経路:C3からC3bBbPのもつC3 convertase活性により生成し、n(C3bBb)はC5 convertase活性を持つ (2008前期免疫学プリント 68)
  • 別経路では細菌の表面でC3bが安定的に存在→オプソニン作用を有する


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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/09/18 15:57:51」(JST)

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英文文献

  • Mechanisms of enhanced neutralization of botulinum neurotoxin by monoclonal antibodies conjugated to antibodies specific for the erythrocyte complement receptor.
  • Sharma R, Zhao H, Al-Saleem FH, Ubaid AS, Puligedda RD, Segan AT, Lindorfer MA, Bermudez R, Elias M, Adekar SP, Simpson LL, Taylor RP, Dessain SK.Author information Lankenau Institute for Medical Research, Wynnewood, PA 19096, USA.AbstractImmune complexes formed between monoclonal antibodies (mAbs) and toxins can neutralize toxicity in vivo by multiple mechanisms. Toxin sequestration and clearance by mAbs may be improved by enhancing their ability to bind to red blood cells (RBCs) through immune adherence. This can be achieved by converting the mAbs to heteropolymers (HPs), which are antigen-specific mAbs cross-linked to mAbs targeting the complement receptor (CR1), a protein that is expressed on the surface of RBCs in primates and mediates delivery of complement C3b-containing immune complexes to tissue macrophages. Conversion of mAbs to HPs has been shown to enhance clearance of multivalent antigens from the blood circulation, but the interaction of HPs with monovalent toxins has not been examined. Using botulinum neurotoxin (BoNT) as a model system, we studied the effect of conversion of a pair of BoNT-specific mAbs into HPs on toxin neutralization and handling in vivo. Two HPs given in combination had 166-fold greater potency than un-modified mAbs, neutralizing 5000 LD50 BoNT, when tested in transgenic mice expressing human CR1 on RBC membranes. Improvement required adherence of BoNT to the RBC in vivo and 2 HPs, rather than an HP+mAb pair. The HP pair bound BoNT to RBCs in the circulation for 2h, in comparison to BoNT-neutralizing anti-serum, which induced no detectable RBC binding. HP pairs exhibited enhanced uptake by peritoneal macrophages in vitro, compared to pairs of mAbs or mAb+HP pairs. In a post-exposure therapeutic model, HPs gave complete protection from a lethal BoNT dose up to 3h after toxin exposure. In a pre-exposure prophylaxis model, mice given HP up to 5 days prior to BoNT administration were fully protected from a lethal BoNT dose. These studies elucidate general mechanisms for the neutralization of toxins by HP pairs and demonstrate the potential utility of HPs as BoNT therapeutics.
  • Molecular immunology.Mol Immunol.2014 Feb;57(2):247-54. doi: 10.1016/j.molimm.2013.09.005. Epub 2013 Nov 1.
  • Immune complexes formed between monoclonal antibodies (mAbs) and toxins can neutralize toxicity in vivo by multiple mechanisms. Toxin sequestration and clearance by mAbs may be improved by enhancing their ability to bind to red blood cells (RBCs) through immune adherence. This can be achieved by con
  • PMID 24184879
  • Versatile Roles of CspA Orthologs in Complement Inactivation of Serum-Resistant Lyme Disease Spirochetes.
  • Hammerschmidt C, Koenigs A, Siegel C, Hallström T, Skerka C, Wallich R, Zipfel PF, Kraiczy P.Author information Institute of Medical Microbiology and Infection Control, University Hospital of Frankfurt, Frankfurt, Germany.AbstractCspA of the Lyme disease spirochete Borrelia burgdorferi represents a key molecule in immune evasion, protecting borrelial cells from complement-mediated killing. As previous studies focused almost exclusively on CspA of B. burgdorferi, here we investigate the different binding capacities of CspA orthologs of Borrelia burgdorferi, B. afzelii, and B. spielmanii for complement regulator factor H and plasminogen and their ability to inhibit complement activation by either binding these host-derived plasma proteins or independently by direct interaction with components involved in formation of the lethal, pore-like terminal complement complex. To further examine their function in serum resistance in vivo, a serum-sensitive B. garinii strain was used to generate spirochetes, ectopically producing functional CspA orthologs. Irrespective of their species origin, all three CspA orthologs impart resistance to complement-mediated killing when produced in a serum-sensitive B. garinii surrogate strain. To analyze the inhibitory effect on complement activation and to assess the potential to inactivate C3b by binding of factor H and plasminogen, recombinant CspA orthologs were also investigated. All three CspA orthologs simultaneously bound factor H and plasminogen but differed in regard to their capacity to inactivate C3b via bound plasmin(ogen) and inhibit formation of the terminal complement complex. CspA of B. afzelii binds plasmin(ogen) and inhibits the terminal complement complex more efficiently than CspA of B. burgdorferi and B. spielmanii. Taken together, CspA orthologs of serum-resistant Lyme disease spirochetes act as multifunctional evasion molecules that inhibit complement on two central activation levels, C3b generation and assembly of the terminal complement complex.
  • Infection and immunity.Infect Immun.2014 Jan;82(1):380-92. doi: 10.1128/IAI.01094-13. Epub 2013 Nov 4.
  • CspA of the Lyme disease spirochete Borrelia burgdorferi represents a key molecule in immune evasion, protecting borrelial cells from complement-mediated killing. As previous studies focused almost exclusively on CspA of B. burgdorferi, here we investigate the different binding capacities of CspA or
  • PMID 24191298
  • Detection of cell membrane-bound CD46 using flow cytometry.
  • Kolev M, Kemper C.Author information Division of Transplantation Immunology and Mucosal Biology, MRC Centre for Transplantation, King's College London, Guy's Hospital, London, UK.AbstractCD46 is an important regulator of the complement system by preventing unwanted deposition of the complement activation products and opsonins C3b/C4b onto self-tissue. Recently, intracellular signals mediated by CD46 activation on several distinct human cell types have demonstrated that CD46 also plays decisive roles in immuneregulation. The growing recognition of CD46 as key regulator in several vital biological processes, led to increased demand in sensitive methods for monitoring CD46 expression and changes thereof on cells and in tissues. Here we describe a method, which allows for studying CD46 expression on the surface of cells using specific antibodies in combination with fluorescence-activated cell sorting (FACS) analysis.
  • Methods in molecular biology (Clifton, N.J.).Methods Mol Biol.2014;1100:329-39. doi: 10.1007/978-1-62703-724-2_27.
  • CD46 is an important regulator of the complement system by preventing unwanted deposition of the complement activation products and opsonins C3b/C4b onto self-tissue. Recently, intracellular signals mediated by CD46 activation on several distinct human cell types have demonstrated that CD46 also pla
  • PMID 24218272

和文文献

  • 緑藻 クロレラ Chlorella pyrenoidosa より得られたペプチドヘテロ多糖体の補体 C3 と腹腔マクロファージに及ぼす影響
  • 寒冷凝集素症
  • Effects of endosulfan on the immune function of erythrocytes, and potential protection by testosterone propionate

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★リンクテーブル★
先読み補体
リンク元食細胞」「D因子
拡張検索C3b inactivator deficiency
関連記事C」「C3

補体」

  [★]

complement
アレキシン alexin
補体活性化経路補体価


  • 図:IMM.63
pathway start first step
classical pathway antigen-antibody complex C1q, C1r, C1s, C4, C2
lectin pathway mannose-binding lectin or ficolin binds carbohydrate on pathogen surface MBL/ficolin, MASP-2, C4, C2
alternative pathway pathogen surface C3, B, D

補体の相互作用 IMM.62

  • C1qがカスケードの最初となる。3つの方法で補体カスケードがはじまる。
  • (1)多価陰イオン表面(例えば、グラム陰性細菌のリポテイコ酸)
  • (2)バクテリアの多糖のホスホコリンに結合(例えば肺炎球菌のC蛋白質)
  • (3)抗原抗体複合体に結合して自然免疫と獲得免疫のエフェクター機構を結びつける。
  • 炭化水素鎖を認識するレクチンがカスケードの最初となる。
  • C3からはじまる。血漿中のC3が病原体の表面で自発的に活性化されることで補体反応がはじまる。
3つの経路は共通してC3 convertaseを生成。C3 convertaseはC3→C3a+C3b
C3a: C3a is a peptide mediator of local inflammation
C3b: C3b binds covalently to the bacterial cell membrane and opsonizes the bacteria
C5 convertaseはC3bにC3 convertaseが結合してできる
C5 converaseはC5→C5a+C5b
C5a: powerful peptide mediator of inflammation
C5b: C5b,C6,C7,C8,C9: membrane-attack complex

C3aとC5a。C4a

炎症部位に血管外に抗体、補体、食細胞を集め、組織液を増やすことで抗原提示細胞がリンパ節に移動するのを促進する(IMM.75)
  • C5a,C3a,C4a: smooth muscle contraction.(IMM.75)
  • C5a,C3a: act on the endo thelial cells lining blood vessels to induce adhesion molecules.(IMM.75)
  • C5a>C3a>C4a: increase in blood flow, increase vascular permeability, increase binding of phagocytes to exdothielial cells.(IMM.76)
  • C5a: activates mast cells to release mediators, such as histamine and TNF-α. that contribute the inflammatory response(IMM.76).
  • C5a: acts directly on neutrophils and monocytes and attracting neutrophils and monocytes(IMM.75)
  • C3a: contributes to the pypotension and edema seen in endotoxic shock
  • C5a: activated by endotoxin, funcions in neutrophil chemotaxis

C5a

臨床関連

  • 増加:



食細胞」

  [★]

phagocyte
貪食細胞
[show details]


食細胞表面レセプター (SMB.38)

リガンド種 受容体 CD リガンド 発現
抗体 FcγRI CD64 IgG3, IgG1, IgG4 マクロファージ
FcγRII CD32 IgG3, IgG1, IgG2 多核白血球
FcγRIII CD16 IgG1, IgG3  
補体 CR1 CD35 C3b  
CR3 CD11b/CD18 iC3b  
CR4 CD11c/CD18 iC3b  


D因子」

  [★]

factor D, D
C3プロアクチベーター転換酵素活性化D因子
第二経路C3, C3b, B, C3bBb, C3a


C3b inactivator deficiency」

  [★] C3b不活性化因子欠損症

C」

  [★]

WordNet   license wordnet

「the 3rd letter of the Roman alphabet」
c

WordNet   license wordnet

「(music) the keynote of the scale of C major」

WordNet   license wordnet

「a general-purpose programing language closely associated with the UNIX operating system」

PrepTutorEJDIC   license prepejdic

「carbonの化学記号」

C3」

  [★]

補体第三成分 third component of complement
補体C3a, C3b
  • 補体の一つ
  • C3は血清中に最も多く存在する
  • C3 convertaseによってC3aC3bを生じる
  • C3 convertase活性を持つのは2つ
1. C4bC2a (古典的経路)
2. C3bBbP (別経路)



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