崩壊促進因子, DAF, decay-accelerating factor
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/08/04 08:47:51」(JST)
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| CD55 molecule, decay accelerating factor for complement (Cromer blood group) |
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PDB rendering based on 1h03.
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| Available structures |
| PDB |
Ortholog search: PDBe, RCSB |
| List of PDB id codes |
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1H03, 1H04, 1H2P, 1H2Q, 1M11, 1NWV, 1OJV, 1OJW, 1OJY, 1OK1, 1OK2, 1OK3, 1OK9, 1UOT, 1UPN, 2C8I, 2QZD, 2QZF, 2QZH, 3IYP, 3J24
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| Identifiers |
| Symbols |
CD55 ; CR; CROM; DAF; TC |
| External IDs |
OMIM: 125240 MGI: 104850 HomoloGene: 479 GeneCards: CD55 Gene |
| Gene ontology |
| Molecular function |
• virus receptor activity
• protein binding
• lipid binding
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| Cellular component |
• extracellular region
• cytosol
• plasma membrane
• integral component of plasma membrane
• cell surface
• anchored component of membrane
• membrane raft
• extracellular exosome
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| Biological process |
• complement activation, classical pathway
• positive regulation of cytosolic calcium ion concentration
• regulation of complement activation
• regulation of lipopolysaccharide-mediated signaling pathway
• CD4-positive, alpha-beta T cell cytokine production
• innate immune response
• respiratory burst
• negative regulation of complement activation
• viral entry into host cell
• positive regulation of CD4-positive, alpha-beta T cell activation
• positive regulation of CD4-positive, alpha-beta T cell proliferation
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| Sources: Amigo / QuickGO |
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| RNA expression pattern |
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| More reference expression data |
| Orthologs |
| Species |
Human |
Mouse |
| Entrez |
1604 |
13136 |
| Ensembl |
ENSG00000196352 |
ENSMUSG00000026399 |
| UniProt |
P08174 |
Q61475 |
| RefSeq (mRNA) |
NM_000574 |
NM_010016 |
| RefSeq (protein) |
NP_000565 |
NP_034146 |
| Location (UCSC) |
Chr 1:
207.32 – 207.36 Mb |
Chr 1:
130.44 – 130.46 Mb |
| PubMed search |
[1] |
[2] |
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Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene.[1]
Decay accelerating factor is a 70 kDa membrane protein that regulates the complement system on the cell surface. DAF recognizes C4b and C3b fragments that are created during C4 (classical complement pathway and lectin pathway) and C3 (alternate complement pathway) activation. Interaction of DAF with cell-associated C4b and C3b proteins interferes with their ability to catalyze the conversion of C2 and factor B to active C2b (historically called C2a) and Bb and thereby prevents the formation of C4b2b and C3bBb, the amplification convertases of the complement cascade - thus blocking the formation of the membrane attack complex.[2]
This glycoprotein is broadly distributed among hematopoietic and non-hematopoietic cells. It is a determinant for the Cromer blood group system.
Contents
- 1 Pathology
- 1.1 Paroxysmal nocturnal hemoglobinuria
- 1.2 Infectious diseases
- 2 See also
- 3 References
- 4 Further reading
- 5 External links
Pathology
Paroxysmal nocturnal hemoglobinuria
Because DAF is a GPI-anchored protein, its expression is reduced in persons with mutations that reduce GPI levels such as those with paroxysmal nocturnal hemoglobinuria; in that disorder, red blood cells with very low levels of DAF and CD59 undergo complement-mediated hemolysis.[3]
Infectious diseases
DAF is used as a receptor by some coxsackieviruses and other enteroviruses.[4] Recombinant soluble DAF-Fc has been tested in mice as an anti-enterovirus therapy for heart damage;[5] however, the human enterovirus that was tested binds much more strongly to human DAF than to mouse or rat DAF. Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF.[6] and DAF-Fc has yet to be tested in humans.
See also
- List of human clusters of differentiation
- CD59
References
- ^ Medof ME, Lublin DM, Holers VM, Ayers DJ, Getty RR, Leykam JF, Atkinson JP, Tykocinski ML (April 1987). "Cloning and characterization of cDNAs encoding the complete sequence of decay-accelerating factor of human complement". Proc. Natl. Acad. Sci. U.S.A. 84 (7): 2007–11. doi:10.1073/pnas.84.7.2007. PMC 304572. PMID 2436222.
- ^ http://www.genecards.org/cgi-bin/carddisp.pl?gene=CD55#function.
- ^ Parker C, Omine M, Richards S et al. (2005). "Diagnosis and management of paroxysmal nocturnal hemoglobinuria". Blood 106 (12): 3699–709. doi:10.1182/blood-2005-04-1717. PMC 1895106. PMID 16051736.
- ^ Karnauchow TM, Tolson DL, Harrison BA, Altman E, Lublin DM, Dimock K (August 1996). "The HeLa cell receptor for enterovirus 70 is decay-accelerating factor (CD55)". J. Virol. 70 (8): 5143–52. PMC 190469. PMID 8764022.
- ^ Yanagawa B, Spiller OB, Choy J, Luo H, Cheung P, Zhang HM, Goodfellow IG, Evans DJ, Suarez A, Yang D, McManus BM (January 2003). "Coxsackievirus B3-associated myocardial pathology and viral load reduced by recombinant soluble human decay-accelerating factor in mice". Lab. Invest. 83 (1): 75–85. doi:10.1097/01.lab.0000049349.56211.09. PMID 12533688.
- ^ Spiller OB, Goodfellow IG, Evans DJ, Almond JW, Morgan BP (January 2000). "Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF". J. Infect. Dis. 181 (1): 340–3. doi:10.1086/315210. PMID 10608785.
Further reading
- Selinka HC, Wolde A, Sauter M et al. (2004). "Virus-receptor interactions of coxsackie B viruses and their putative influence on cardiotropism.". Med. Microbiol. Immunol. 193 (2-3): 127–31. doi:10.1007/s00430-003-0193-y. PMID 12920584.
- Mikesch JH, Schier K, Roetger A et al. (2007). "The expression and action of decay-accelerating factor (CD55) in human malignancies and cancer therapy.". Cell. Oncol. 28 (5-6): 223–32. PMID 17167176.
External links
- Decay-Accelerating Factor at the US National Library of Medicine Medical Subject Headings (MeSH)
- Cromer blood group system at BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH
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PDB gallery
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1h03: HUMAN CD55 DOMAINS 3 & 4
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1h04: HUMAN CD55 DOMAINS 3 & 4
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1h2p: HUMAN CD55 DOMAINS 3 & 4
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1h2q: HUMAN CD55 DOMAINS 3 & 4
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1nwv: SOLUTION STRUCTURE OF A FUNCTIONALLY ACTIVE COMPONENT OF DECAY ACCELERATING FACTOR
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1ojv: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ojw: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ojy: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ok1: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ok2: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ok3: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1ok9: DECAY ACCELERATING FACTOR (CD55): THE STRUCTURE OF AN INTACT HUMAN COMPLEMENT REGULATOR.
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1uot: HUMAN CD55 DOMAINS 3 & 4
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1upn: COMPLEX OF ECHOVIRUS TYPE 12 WITH DOMAINS 3 AND 4 OF ITS RECEPTOR DECAY ACCELERATING FACTOR (CD55) BY CRYO ELECTRON MICROSCOPY AT 16 A
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Proteins: complement system (C, L, A)
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| Activators/enzymes |
| Early |
- A: Factor B
- Factor D
- Factor P/Properdin
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| Middle |
- C3-convertase
- C5-convertase
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| Late |
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| Inhibitors |
- CLA: C1-inhibitor
- Decay-accelerating factor/CD59
- Factor I
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| Complement receptors |
- CR1
- CR2
- CR3
- CR4
- CD11b/CD11c/CD18
- Anaphylatoxin
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Index of the immune system
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| Description |
- Physiology
- cells
- autoantigens
- autoantibodies
- complement
- surface antigens
- IG receptors
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| Disease |
- Allergies
- Immunodeficiency
- Immunoproliferative immunoglobulin disorders
- Hypersensitivity and autoimmune disorders
- Neoplasms and cancer
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| Treatment |
- Procedures
- Drugs
- antihistamines
- immunostimulants
- immunosuppressants
- monoclonal antibodies
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UpToDate Contents
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- 1. 発作性夜間血色素尿症の病因 pathogenesis of paroxysmal nocturnal hemoglobinuria
- 2. 補体系の遺伝性疾患 inherited disorders of the complement system
- 3. 補体系の制御因子および受容体 regulators and receptors of the complement system
- 4. 母体 - 胎児接点の免疫 immunology of the maternal fetal interface
- 5. 発作性夜間血色素尿症の臨床症状および診断 clinical manifestations and diagnosis of paroxysmal nocturnal hemoglobinuria
English Journal
- Oxymatrine protects against l-arginine-induced acute pancreatitis and intestine injury involving Th1/Th17 cytokines and MAPK/NF-κB signalling.
- Zhang Z, Liu Q, Zang H, Shao Q, Sun T.
- Pharmaceutical biology. 2019 Dec;57(1)595-603.
- Array Array Array
- PMID 31496325
- Staphylococcal phosphatidylinositol-specific phospholipase C potentiates lung injury via complement sensitisation.
- Lin YC, Liao YJ, Lee YH, Tseng SF, Liu JY, Chen YS, Shui HA, Lin FZ, Lin KH, Chen YC, Tsai MC, Sytwu HK, Wang CC, Chuang YP.
- Cellular microbiology. 2019 Oct;21(10)e13085.
- Staphylococcus aureus is frequently isolated from patients with community-acquired pneumonia and acute respiratory distress syndrome (ARDS). ARDS is associated with staphylococcal phosphatidylinositol-specific phospholipase C (PI-PLC); however, the role of PI-PLC in the pathogenesis and progression
- PMID 31290210
- The potential role of 3D-bioprinting in xenotransplantation.
- Li P, Zhang W, Smith LJ, Ayares D, Cooper DKC, Ekser B.
- Current opinion in organ transplantation. 2019 Oct;24(5)547-554.
- To review the impact of a new technology, 3D-bioprinting, in xenotransplantation research. Genetically engineered pigs, beginning with human (h) CD55-transgenic and Gal-knockout pigs, have improved the outcomes of xenotransplantation research. Today, there are more than 30 different genetically engi
- PMID 31385888
Japanese Journal
- Comparative Gene Expression Analysis in the Skeletal Muscles of Dysferlin-deficient SJL/J and A/J Mice
- Kobayashi Kinji,Izawa Takeshi,Kuwamura Mitsuru,Yamate Jyoji
- Journal of Toxicologic Pathology 24(1), 49-62, 2011
- … SJL/J mice exhibited a marked lowering of decay-accelerating factor 1/CD55 gene expression level in all studied muscles except for the heart at all ages compared with that of BALB/c mice. …
- NAID 130000675354
- Identification of DAF1/CD55, a novel definitive endoderm marker
- Shiraki Nobuaki,Harada Seiko,Ogaki Soichiro [他]
- Cell Structure and Function 35(1・2), 73-80, 2010-12
- NAID 40018702767
Related Pictures
★リンクテーブル★
[★]
- 英
- paroxysmal nocturnal hemoglobinuria PNH
- 同
- 発作性夜間ヘモグロビン尿症 *難病 http://www.nanbyou.or.jp/sikkan/116_2_i.htm
- マルキアファーヴァ-ミケリ症候群 Marchiafava-Micheli syndrome
- 関
- 難病
- first aid step1 2006 p.187
- red urine in the morning
概念
疫学
原因
- 補体活性化異常、活性化経路制御分子の欠損 → 造血幹細胞レベルの異常
- 発作性夜間血色素尿症 PNH:paroxysmal nocternal hemglobulinemia
- CD55 DAF decay accelerating factor C3b,C5bの酵素阻害
- CD59 HRF homologous restriction factor MAC形成阻害
- =Protectin, Mac inhibitor
- PIG-A GPIアンカー型蛋白質の欠損
病態
- 静脈血栓症：原因は不明。血小板膜上の補体が小胞化による補体複合体の除去を活性化する。循環中に流れ出たこのmicroparticleはホスファチジルセリンに富んでおり、血栓原性が高い。(参考1)
症状
- 貧血、黄疸、夜間の溶血発作（血中CO2濃度の上昇が原因）
合併症
検査
血算
- → 正球性正色素性貧血、慢性経過で鉄が不足し小球性低色素性貧血
- 好中球アルカリフォスファターゼスコア：低値(NAPスコア：低下)
血液生化学
- LDH：上昇
- ハプトグロビン：減少
- 間接ビリルビン：上昇
- 慢性の血管内溶血により鉄が欠乏 → 血清鉄↓、血清フェリチン↓
尿検査
- 血管内溶血によりヘム鉄は糸球体濾過されて、ヘモグロビンは尿細管で再吸収され、鉄はヘモジデリンとして尿中に排泄される。 (ポルフィリンどこいった？)
- 発作時に認められる
治療
- ほとんどの患者で生涯にわたる支持療法(suppertive care)を受ける人が多い。(HIM.661)
- 若い患者で重症のPNHであれば同種骨髄移植を提案すべき(should be offered) (HIM.661)
支持療法
- フィルターで白血球を除去した赤血球製剤を使用。伝統的に溶血を引き起こすwhite cell reaction(白血球に対する抗HLA抗体による抗原抗体反応、のこと？)を防止するために洗浄赤血球が用いられてきたが、これは無駄である。(HIM.661)(also see. 参考2)
- 葉酸
- 鉄剤
- 補体成分C5に対するヒト化モノクローナル抗体 エクリズマブ eclizumab
- ×
糖質コルチコイド：長期にわたる使用におけるエビデンスなし
根治療法
USMLE
参考
- 1. [charged] Clinical manifestations of paroxysmal nocturnal hemoglobinuria - uptodate [1]
- 2. [charged] Diagnosis and treatment of paroxysmal nocturnal hemoglobinuria - uptodate [2]
[★]
- 英
- cluster of differentiation, CD
- Bリンパ球 CD10,CD19,CD20
- Tリンパ球 CD2,CD3,CD5,CD7
- 幹細胞 CD34
- 顆粒球 CD13,CD33
- 単球 CD14：LPSをリガンドとし、Toll-like receptorと共役して細胞内シグナルを伝達する分子。
- 巨核球 CD41(GpIIb),CD42(GpIb)
- NK細胞：CD16(IgGのFc部に対する受容体)、CD56(NCAM-I)
[★]
- 英
- decay-accelerating factor, decay accelerating factor, DAF
- 同
- CD55抗原、CD55
- 関
- CD59、発作性夜間血色素尿症
[★]
崩壊促進因子 DAF CD55
[★]
CD55抗原
- 関
- decay-accelerating factor
[★]
- 英
- CD55 antigen
- 関
- 崩壊促進因子
[★]
- 同
- Leucine-1
発現細胞
- 胸腺細胞、T細胞、B細胞のサブセット (IMM)
- 胸腺細胞、T細胞、NK細胞、B1(B細胞のsubpopulation) (WCH.31)
- 成熟T細胞、胸腺細胞、一部のB細胞(CD5陽性B細胞(B-1細胞)。脾臓等、異所由来(骨髄非依存性)のB細胞) (資料1)
- B細胞性白血病・リンパ腫(資料1)
分子量
別名
機能
- CD5に対するモノクローナル抗体を作用させると、細胞内のチロシンのリン酸化が起こり、T細胞が活性化する。ただし、抑制的に作用する経路にも作用するかもしれない(WCH.31)
- CD5+ B細胞は自己抗体を産生する(WCH.31)
- CD72はCD5にたいするcounter-receptorである(WCH.31)
臨床関連
参考
- http://www.srl.info/srlinfo/kensa_ref_CD/KENSA/SRL5039.htm
- http://www.bc-cytometry.com/Data/db_search/CD005.htm
[★]