- 関
- CD11b:CD18 (integrin αMβ2:Mac-1)
- 同
- CDllb
- 関
- CD11b:CD18 (integrin αMβ2:Mac-1)
WordNet
- the 13th letter of the Roman alphabet (同)m
PrepTutorEJDIC
- おい,君,名前の分からない相手（男）に対して呼びかけるときに使う, Apple社のMacintoshコンピューター
- Mach number / mark[s] / Monsieur
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/26 10:49:23」(JST)
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- 1. 補体系の制御因子および受容体 regulators and receptors of the complement system
- 2. 炎症の病因における白血球内皮細胞接着 leukocyte endothelial adhesion in the pathogenesis of inflammation
- 3. 白血球粘着不全症 leukocyte adhesion deficiency
- 4. 補体系の遺伝性疾患 inherited disorders of the complement system
- 5. 免疫グロブリンの機能および臨床応用 function and clinical applications of immunoglobulins
English Journal
- Expression and cell distribution of receptor for advanced glycation end-products in the rat cortex following experimental subarachnoid hemorrhage.
- Li H1, Wu W1, Sun Q1, Liu M2, Li W1, Zhang XS3, Zhou ML1, Hang CH4.Author information 1Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, China.2Department of Neurosurgery, School of Medicine, Southern Medical University (Guangzhou), Jinling Hospital, Nanjing, Jiangsu Province, China.3Department of Neurosurgery, School of Medicine, Second Military Medical University (Shanghai), Jinling Hospital, Nanjing, Jiangsu Province, China.4Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, China. Electronic address: hang_neurosurgery@163.com.AbstractConvincing evidence indicates that inflammation contributes to the adverse prognosis of subarachnoid hemorrhage (SAH). Some pro-inflammatory molecules such as high mobility group protein 1, S100 family of proteins, β-amyloid peptide, and macrophage antigen complex 1 have been involved in the damaging inflammation process following SAH. The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor that senses these molecules and plays central role in inflammatory processes. This study aimed to determine the expression and cell distribution of RAGE in the brain cortex after SAH. Male Sprague-Dawley rats were randomly divided into sham group and SAH groups at 6h, 12h and on day 1, day 2 and day 3 (n=6 for each subgroup). SAH groups suffered experimental SAH by injection of 0.3ml autologous blood into the prechiasmatic cistern. RAGE expression was measured by Western blot, real-time PCR, immunohistochemistry and immunofluorescence. Nuclear expression of p65 protein, the major subunit of nuclear factor kappa B, was also detected. Our data demonstrated that the expression levels of RAGE and nuclear p65 protein were both markedly increased after SAH. Moreover, there was a significant positive correlation between the expression of RAGE and that of p65 protein. Double immunofluorescence staining showed that RAGE was expressed by neuron and microglia rather than astrocyte after SAH. These results suggest that RAGE may be directly involved in the inflammatory response after SAH, and there might be important implications for further studies using specific RAGE antagonists to decrease inflammation-mediated brain injury following SAH.
- Brain research.Brain Res.2014 Jan 16;1543:315-23. doi: 10.1016/j.brainres.2013.11.023. Epub 2013 Nov 26.
- Convincing evidence indicates that inflammation contributes to the adverse prognosis of subarachnoid hemorrhage (SAH). Some pro-inflammatory molecules such as high mobility group protein 1, S100 family of proteins, β-amyloid peptide, and macrophage antigen complex 1 have been involved in the damagi
- PMID 24291745
- Postprandial VLDL lipolysis products increase monocyte adhesion and lipid droplet formation via activation of ERK2 and NFκB.
- den Hartigh LJ, Altman R, Norman JE, Rutledge JC.Author information Department of Internal Medicine, Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, University of California, Davis, California;AbstractPostprandial lipemia is characterized by a transient increase in circulating triglyceride-rich lipoproteins such as very low-density lipoprotein (VLDL) and has been shown to activate monocytes in vivo. Lipolysis of VLDL releases remnant particles, phospholipids, monoglycerides, diglycerides, and fatty acids in close proximity to endothelial cells and monocytes. We hypothesized that postprandial VLDL lipolysis products could activate and recruit monocytes by increasing monocyte expression of proinflammatory cytokines and adhesion molecules, and that such activation is related to the development of lipid droplets. Freshly isolated human monocytes were treated with VLDL lipolysis products (2.28 mmol/l triglycerides + 2 U/ml lipoprotein lipase), and monocyte adhesion to a primed endothelial monolayer was observed using a parallel plate flow chamber coupled with a CCD camera. Treated monocytes showed more rolling and adhesion than controls, and an increase in transmigration between endothelial cells. The increased adhesive events were related to elevated expression of key integrin complexes including Mac-1 [αm-integrin (CD11b)/β2-integrin (CD18)], CR4 [αx-integrin (CD11c)/CD18] and VLA-4 [α4-integrin (CD49d)/β1-integrin (CD29)] on treated monocytes. Treatment of peripheral blood mononuclear cells (PBMCs) and THP-1 monocytes with VLDL lipolysis products increased expression of TNFα, IL-1β, and IL-8 over controls, with concurrent activation of NFkB and AP-1. NFκB and AP-1-induced cytokine and integrin expression was dependent on ERK and Akt phosphorylation. Additionally, fatty acids from VLDL lipolysis products induced ERK2-dependent lipid droplet formation in monocytes, suggesting a link to inflammatory signaling pathways. These results provide novel mechanisms for postprandial monocyte activation by VLDL lipolysis products, suggesting new pathways and biomarkers for chronic, intermittent vascular injury.
- American journal of physiology. Heart and circulatory physiology.Am J Physiol Heart Circ Physiol.2014 Jan;306(1):H109-20. doi: 10.1152/ajpheart.00137.2013. Epub 2013 Oct 25.
- Postprandial lipemia is characterized by a transient increase in circulating triglyceride-rich lipoproteins such as very low-density lipoprotein (VLDL) and has been shown to activate monocytes in vivo. Lipolysis of VLDL releases remnant particles, phospholipids, monoglycerides, diglycerides, and fat
- PMID 24163071
- β2 Integrin-Mediated Crawling on Endothelial ICAM-1 and ICAM-2 Is a Prerequisite for Transcellular Neutrophil Diapedesis across the Inflamed Blood-Brain Barrier.
- Gorina R, Lyck R, Vestweber D, Engelhardt B.Author information Theodor Kocher Institute, University of Bern, Bern CH-3012, Switzerland.AbstractIn acute neuroinflammatory states such as meningitis, neutrophils cross the blood-brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of neutrophils from wild-type, CD11a(-/-), CD11b(-/-), and CD18(null) mice with wild-type, junctional adhesion molecule-A(-/-), ICAM-1(null), ICAM-2(-/-) , or ICAM-1(null)/ICAM-2(-/-) primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein-coupled receptor-dependent activation of β2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, β2 integrin-mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB.
- Journal of immunology (Baltimore, Md. : 1950).J Immunol.2014 Jan 1;192(1):324-37. doi: 10.4049/jimmunol.1300858. Epub 2013 Nov 20.
- In acute neuroinflammatory states such as meningitis, neutrophils cross the blood-brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated
- PMID 24259506
Japanese Journal
- C3レセプター(CR1,2,3,4) (広範囲 血液・尿化学検査 免疫学的検査(第7版・3)その数値をどう読むか) -- (免疫学的検査 補体および関連物質)
- 若狭 健太郎,瀬谷 司
- 日本臨床 68(-) (980), 68-72, 2010-06
- NAID 40017181708
- Immunohistochemical Examination on the Distribution of Cells Expressed Lymphatic Endothelial Marker Podoplanin and LYVE-1 in the Mouse Tongue Tissue
- Noda Yuya,Amano Ikuko,Hata Minoru,Kojima Hiroshi,Sawa Yoshihiko
- ACTA HISTOCHEMICA ET CYTOCHEMICA advpub(0), 1004020081, 2010
- … Recently, it has been reported that several tissue cells and leukocytes express lymphatic markers, LYVE-1 and podoplanin. … This study was aimed to clarify the lingual distribution of cells expressing LYVE-1 and podoplanin. … LYVE-1 is expressed in the macrophage marker Mac-1-positive cells as well as lymphatic vessels, while factor-VIII was detected in only blood endothelial cells. …
- NAID 130000248643
Related Links
- マウス抗原に対する抗体（CD抗体） CD11b(Mac-1) CD11bは、3型補体レセプタ（CR3）としても知られ、インテグリンβ2（CD18）分子と会合してMac-1ヘテロダイマーを形成するインテグリンαMサブユニットです。腹腔や胸腔の顆粒球 ...
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Related Pictures
★リンクテーブル★
| リンク元 | 「接着分子」「白血球」「インテグリン」「白血球粘着不全症」「ICAM-1」 |
| 関連記事 | 「MAC」「Mac」「M」 |
「接着分子」
- 英
- adhesion molecule
- 同
- 接着因子
- 関
接着分子のファミリー
白血球の相互作用に関与している接着分子 (IMM.87)
| グループ名 | 機能 | 名称 | 別名 | 組織分布 | リガンド | |
| セレクチン | 炭化水素鎖に結合。 白血球-内皮細胞の反応を開始 |
P-selectin | PADGEN | CD62P | 活性化した内皮細胞、活性化した血小板 | PSGL-1, sialyl-Lewisx |
| E-selectin | ELAM-1 | CD62E | 活性化した内皮細胞 | sialyl-Lewisx | ||
| インテグリン | CAMや細胞外マトリックスに結合。 強い結合 |
LFA-1 | αL:β2 | CD11a:CD18 | 単球、T細胞、マクロファージ、好中球、樹状細胞 | ICAMs |
| CR3, Mac-1 | αM:β2 | CD11b:CD18 | 好中球、単球、マクロファージ | ICAM-1, iC3b, fibrinogen | ||
| CR4, p150.95 | αX:β2 | CD11c:CD18 | 樹状細胞、マクロファージ、好中球 | iC3b | ||
| VLA-5 | α5:β1 | CD49d:CD29 | 単球、マクロファージ | fibronectin | ||
| 免疫グロブリンスーパーファミリー | 細胞結合で様々に働く。 インテグリンの基質 |
ICAM-1 | CD54 | 活性化した内皮細胞 | LFA-1, MAC1 | |
| ICAM-2 | CD102 | 非活性化状態の内皮細胞、樹状細胞 | LFA-1 | |||
| VCAM-1 | CD106 | 活性化した内皮細胞 | VLA-4 | |||
| PECAM | CD31 | 活性化した白血球、内皮細胞間の結合 | CD31 | |||
白血球の相互作用に関与している免疫グロブリンスーパーファミリーの接着分子 (IMM.329)
| 名称 | 分布組織 | リガンド | ||
| CD2 | LFA-2 | T細胞 | LFA-1 | CD53 |
| ICAM-1 | CD54 | 活性化した血管、リンパ球、樹状細胞 | LFA-1, Mac-1 | |
| ICAM-2 | CD102 | 非活性化状態の血管 | LFA-1 | |
| ICAM-3 | CD50 | Naive T cells | DC-SIGN, LFA-1 | |
| LFA-3 | CD58 | リンパ球、APC | CD2 | |
| VCAM-1 | CD106 | 活性化した内皮細胞 | VLA-4 | |
-接着分子
-細胞接着分子
-カドヘリン
「白血球」
- 英
- leukocyte, leucocyte (Z), white blood cell (Z), WBC, white corpuscle, white cell
- 関
- 赤血球、血球、血液
白血球
基準値
- 4000-9000 (/μl) (2007前期解剖学授業プリント)
- 異常値の出るメカニズム第5版
- 5000- 8400 (/μl) (健常者の2/3)
- 4500-11000 (/μl) (95%範囲)
年齢との関連
- 新生児期>幼児期>成人期(20歳までに成人値)
- 妊婦でも増加(妊娠#妊娠による変化)
生理的な変動
- 精神的ストレス↑ → 交感神経の刺激により好中球の血管壁遊離が促進されるため
- 午前↓、午後↑
基準値
| 07解 | 異メ | 流マ | HIM.A-1 | ||||
| 顆粒球 | 好中球 | 桿状核球 | 40～70 | 44～66 | 40～60 | 4～14 | 0～5 |
| 分葉核球 | 43～59 | 40～70 | |||||
| 好酸球 | 2～4 | 0～ 4 | 2～4 | 0～6 | |||
| 好塩基球 | 0～2 | 0～0.5 | 0～2 | 0～2 | |||
| 無顆粒球 | リンパ球 | 25～40 | 30～38 | 26～40 | 20～50 | ||
| 単球 | 3～6 | 0～ 5 | 3～6 | 4～8 | |||
- 07解: 2007前期解剖学授業プリント
- 異メ: 異常値の出るメカニズム第5版 p.91
- 流マ: 流れが分かる実践検査マニュアル上巻 p.10
血管外滲出 extravasation (SMB.37 BPT.37)
(margination)
- 1. 赤血球は軽く早く流れるので血管の中央をながれ、白血球は血管のへりを流れている
(rolling)
- 2. IL-1, TNFで血管内皮細胞が活性化し、血管内腔にE-selectinを発現する
- 3. P-selectinはヒスタミンやトロンビンの働きにより、血管内腔に発現する
- 4. 白血球と血管内皮細胞の接着分子で接着することで、白血球がrollingを始める
- 3. 次第にselectinによる接着はdown regulateされる
(adheresion & arrested)
- 4. 炎症部位から出されたケモカインが血管内皮細胞の表面ののペプチドグリカンに結合し、白血球に提示される
- 5. 白血球表面のインテグリンが活性化し、血管内皮細胞のICAM-1, VCAM-1と強く結合する
(transmigration)
| 血管内皮細胞 | 白血球 | |
| Rolling | ||
| E-selectin | － | 糖鎖(SLex) |
| P-selectin | － | 糖鎖 |
| 糖鎖(GlyCAM-1)(=CD34) | － | L-selectin |
| Adhestion | ||
| ICAM-1 | － | LFA-1 integlin(CD11a/CD18), Mac-1 integlin(CD11b/CD18) |
| VCAM-1 | － | VLA-1 integlin |
| transmigration | ||
| PECAM-1(CD31) | － | PECAM-1(CD31) |
白血球の染色
- 好酸性：赤く染まる→ヘモグロビン
- 好塩基性：青く染まる→リボソーム、核内のヒストン蛋白
- 好酸性でも好塩基性でもない：淡いピンクに染まる
- MPO myeloperoxidase反応（染色）
- MPOをもつ：顆粒球（前骨髄球～分葉核球）、単球（前単球～単球）
- MPOをもたない：リンパ球系細胞
- 好中球：長鎖エステルを分解
- 単球：短鎖エステルを分解
関節液
- 炎症 感染
- 200 2000 20000
- 500 5000 50000
臨床関連
- LAD(leukocyte adhesion deficiency)症候群 (SMB.37)
- 白血球のインテグリンが欠損または減少する先天性疾患
- 反復性の細菌皮膚感染
- SIRSの診断基準：＜4,000/ul or ＞12,000/ul
「インテグリン」
インテグリン IMM.87
| name | tissue distribution | ligand | ||||||
| 単球 | T細胞 | マクロファージ | 好中球 | 樹状細胞 | ||||
| αL:β2 | LFA-1 | CD11a:CD18 | ○ | ○ | ○ | ○ | ○ | ICAMs |
| αM:β2 | CR3, Mac-1 | CD11b:CD18 | ○ | ○ | ○ | ICAM-1, iC3b, fibrinogen | ||
| αｘ:β2 | CR4, p150.90 | CD11c:CD18 | ○ | ○ | ○ | iC3b | ||
| α5:β1 | VLA-5 | CD49d:CD29 | ○ | ○ | fibronectin | |||
「白血球粘着不全症」
- 好中球機能異常症 phagocytic cell deficiency
概念
病因
- 遺伝子異常により、白血球における接着分子の発現異常を来すことによる
-
- セレクチンのリガンド；ルイス型糖鎖の欠損：type II
疫学
遺伝
病態
- 白血球表面の接着分子 → 感染炎症部位に白血球が浸潤不能 → 感染症遷延
症状
- 生後すぐに反復感染する
- 化膿性細菌や真菌への重篤な感染症。難治性の皮膚感染、中耳炎、副鼻腔炎などの反復感染
- delayed separation of umbilicus
診断
検査
- 白血球数：増多 ← 持続性の顆粒球増多症
- 好中球数：正常
治療
予後
予防
「ICAM-1」
- 同
- intercellular adhesion molecule 1
- 関
- ICAM、ICAM-1:CD54
「MAC」
- 僧帽弁輪石灰化 mitral annular calcification
- 最小肺胞内濃度 minimum alveolar concentration
- 膜攻撃複合体 membrane attack complex
- Mycobacterium avium complex
- 監視下鎮静管理 monitored anesthesia care
- 哺乳類人工染色体 mammalian artificial chromosome
「Mac」