嗜酸性粒细胞和嗜碱性粒细胞计

范文一：嗜酸性粒细胞和嗜碱性粒细胞计数

（一）嗜酸性粒细胞计数嗜酸性粒细胞参与Ⅰ型变态反应，因此嗜酸性粒细胞增多可作为Ⅰ型变态反应的辅助诊断指标，而且可作为疗效判定的指标之一。嗜酸性粒细胞计数可用白细胞分类计数法，也可以用直接计数法，目前多采用后者。该类细胞的胞浆颗粒中富含碱性氨基酸和碱性蛋白，其等电点为pH11，因此呈嗜酸性，易与阴离子结合而被染色。常用的染色液含伊红、石炭酸和福尔马林，该溶液可溶解红细胞和其他白细胞，增加背景的清晰度，使嗜酸性粒细胞易于识别。（二）嗜碱性粒细胞计数嗜碱性粒细胞亦参与Ⅰ型变态反应，其计数方法主要是直接计数法。嗜碱性粒细胞胞浆颗粒中肝素的硫酸根容易与阳离子染料结合而着色，现在常用的酸性染色液包括0.1％EDTA、阿利新蓝、氯代十六烷基吡啶和氯化镧等。该染液能使红细胞和其他白细胞溶解，使嗜酸性粒细胞易于区别。外周血嗜碱性粒细胞数大于33／mm3判为增高，大于50／mm3为显著增高。本试验可作为Ⅰ型变态反应的筛选试验，阳性率可达60％～70％；而且可作为疗效考查的辅助指标。

范文二：嗜碱性粒细胞激发试验的临床应用

山东医２０１药４第年５卷４第３　

嗜期性粒碱胞细激试验发的临应用床

　晓朱敏　，张云慧　，何衡　

韶

（南京１医科大第一学附属医院，京２南０１２０９；２苏州市城人相民医院　；３海南学医）院　摘要：目的

　观察碱性嗜粒细胞激发验试（ＢＴＡ）临的应床用况情，过为疾敏的诊病提断供参。考方法选　择

１

０种人吸性过敏原３对例过０性敏病疾者患行敏原过体外异性Ｂ特ＴＡ，福克全自动过原敏定量分析系统测患者检　清血特异性Ｉｇ（ＥｓｌｇＥ）水平对Ｂ。ＴＡ与ｓｌｇ检测Ｅ结果进一致性行验。结果检　被检１０过种敏原，中马上皮、格链　孢属、孢枝霉属菌、蒿艾、桦白及梯牧草树ＢＡＴ的性阳检出率明高显于清血ｓｌｇ检测ＥＰ，

断过诊敏刚才刚步，起对中人国群的诊疗值还价　需量临床大验数试据临床跟踪和资料才能进一评　步价。

我实　验室自２０１０年６月引进Ｈｉｔｓａｒｅａｄｅｒ５　０１　统系，该检测系统对敏原过的检测方法我与目们　传前使统用通过的体外定性、半定量、定检量测患血　者清特异性Ｉｇ水Ｅ平方法完全同不过。敏反的应应效　段是阶由于体人肥内大细胞过敏原激被活后，引　起肥大细胞脱颗粒，释放出肥大细胞特异类性胰蛋白　

０．７

５一性较好。Ｐ ≤致Ｏ０．５为异有差计统意学义。

２　结果

　ＢＡＴ果结示显，屋尘螨、粉尘螨、链孢格及属　

枝孢属霉菌过敏原检出性阳在２率５％以上；过敏　原ｓＩｇＥ检测结果显示仅，屋尘螨、尘粉阳性螨率高达

　０％５和４６．％，７余其敏过原性检阳率出均在６．７％以　下；上述两种法方测结检阳果吻合性率最的高　过敏原屋尘是和粉尘螨螨分别，１为％和１７３，其余％　过

敏阳性吻合原均率低于％，７上述种方两检法测　屋螨、尘粉尘螨过原敏性阴合吻率均为３７，％而其　他过敏原

阴性合率吻均在３６％以上；两种检测方法

酶组和胺生物活等性介质，引起滑平肌收缩，毛细　血

管扩张通透，性加等，而增产生一的系列敏过症。状　

对过原检敏测整体的阳性率分为别２３％、１２．２％，

Ｐ＜　０．０５两；检测种法方对０种１过敏原的测检结　

果Ｂ

ＴＡ检原测是理在外体模拟体内过敏了反应的　过程，即过用敏激原发者患血中全嗜性粒细碱胞，引　

嗜起碱性粒细胞颗脱粒，组胺释放，释对放组胺的进行　９

山东医２药１０４第年５４卷第３期测　定，确定患是否者对某过种敏物质过。敏清　血ＩｓｇＥ检测目前是对ＩｇＥ介导的过敏反应用运最广　泛

［３］Ｇａｖｒｅｙ　Ｌ，ＫＨｒｏｉｇａａｒｄ　Ｍ，Ｐｏｕｌｓｅｎ　ＬＫ，ｅ　ｔ１．ＩａＥｇ— ｍｅｄｉｔｅｄ　ａａｌｌｅｒｇｙ　ｔｏ　ｈｃｌｏｒｈｅｉｄｉｘｎｅＪ［］．ｌｌＡｅｒ

ｙ　ｇＣｌｉｕ　Ｉｍｍｎｕｏｌ，２００，７１２０（）２４：０９－　

４５１　．

的辅助

断诊法方，点缺对小分是过子原诱敏发的过敏反应几　乎无测意检　Ｊ义。本研对究１种吸人Ｏ性　

敏过原用上述种两检测系统检测，结果二者致一　性较差，原是因种两检测系统检原测理不导同致测　

检［

４Ｍ］ｅｅｒ　ＨｙＷ，ｔＳｈａ　Ｓｋｌｏｖ　Ｐ．Ｏｃｃｕｐａｔｉｏｎａｌ　ｒｈｉｎｓｉｏｎｕｓｉｔｉｓ　ｄｕｅ　ｔｏ　ｔｅｏ —　

ｐ

ｓｏｄｉｅ，ａｎ　ａｎｔｎｉｅｏｐｌｓａｔｉ　ｅａｇｅｎ［ｔＪ．］ｃａＳｎｄＪ　　Ｗｏｒ　Ｅｋｎｖｒｏｎｉ

　ｅｌｔＨａ，ｈ０２１０，３６３（）：２６－６２６７．　

［５］Ｅｂｏ　ＤＧ，Ｂｒｉｄｔｓ　ＨＣ，ＨａｅｇｎｄｏｒｅｎｓＭ　Ｍ，ｔ　ｅ１．ａＢａｓｏｐｈｉｌａ　ｔｃｉａｖｔｉｏｎ　

ｅｔｓｔ　ｙｂ　ｌｆｏｗ　ｃｙｔｏｍｅｔｒｙ：ｒｐｓｅｅｔｎ　ａｎｄ　ｆｕｔｕｅｒａ　ｐｐｌｉａｃｔｉｏｎｓ　ｉｎ　ａｌｌｒｅｏｇｌｏ — 　

结不具相关果性ＢＡＴ。阳性，说明该者患过是因敏　被检过敏原／过源敏活被检患者激的嗜碱性细胞粒　，即过

敏应反的核心效应细胞（碱嗜性粒胞细和肥大　胞）细之一所　致“ Ｊ，而此嗜碱性粒胞细被激活　

的ｇ［ｙＪ］．ＣｙｔｏｍｅｔｒｙＢ　　ＣｉｎｌＣ　ｙｔｏｍ，２０８０，７４（４：２）０１－２１０　．［６

Ｌ］ｏｕｒｅｎｃｏ　ＤＦＡ，ｚｒｏ　ＭＨ，Ｓａｎｔｏｓ　ＪＣｅ，ｔ　ａ１．Ａｔｃｉｖａｔｅｄ　ｔｓａｔｕｓ　ｏｆ　ｂａ　

ｓ－ｏｐｈｉｌ　ｉｓｎ　ｃｈｒｏｉ　ｕｒｉｔｃｒｉａａ　ｌｅａｄｓ　ｔ　ｏｉｎｔｅｌｒｅｕｋｉｎ－－３ｈ　ｙｐｅｒｒｅｓｐｏｎｓｉｖｅ－　－ｅｎｓｓ　ａｎｄ　ｅｎｈａｎｃｅｍｅｔ　ｎｏｆ　ｈｉｓｔａｉｍｎｅ　ｒｌｅａｅｅｓｉ　ｎｕｄｅｃｄｂｙ　ａ　ｎｔｉＩ— Ｅ　ｇ

过程可

能是ＩｇＥ或者ＩｇＧ介导的 ¨　，亦能可是分小　子直接活化式¨方３１Ｈ　

Ｊ或，联合者作用。于过敏对　

原上马皮，格链属孢枝、属孢菌霉，艾蒿，白树及梯桦牧

　ｓ

ｔｉｍｕｌｕｓＪ［］．Ｂｒ　Ｊ　Ｄｅｒｍａｔｌｏ，００８２，１５（５）：８９７９－９８６　．［７Ｂｏ］ｈｍ　ＩＳ，ｐｅｃｋＵ，Ｓ　ｃｈｉｌｄ　ＨＨ．Ｐｉｌｔ　ｏｓｔｕｄｙ　ｏｎ　ｂｓａｏｐｈｉｌ　ｃａｔｖａｉｔｉｏ　ｎ

ｉ

ｎｄｃｅｄｕ　ｕｂｃｏ　ｎｒｔａｓ　ｍｅｔｄｉｍｕ［Ｊ］．Ｆｕｎｄ　ｍＣａｌｉ　ｎＰｈｒａａｃｏｌ，ｍ２０　１１，　２５

２（）：２６７－２７６．　

草ＢＡＴ阳性检率明显高出于ｓＩｇ检测Ｅ，能可是由　于这些过敏原对者患产生的过敏反应为非ｇＩ介导　Ｅ

，故ｓ的Ｉｇ检Ｅ试验测检测到不，而这两者间差的异　有很可能映了反ＩｇＧ介的差异导这，说明ＢＴＡ比

［　８］ＧｏｎａｚｌｚｅｄｅＯ　ｌａｎｏ　Ｄ，Ａｖａｒｅｌｚ　Ｔｗｏｓｅ　，ＭＩｏｒｇａｄｏ　ＪＭｅ，ｔ　ａ１．Ｅｖａｕｌ－ａ

　ｉｔｎｏｏ　ｆ　ｂａｏｓｐｉｌｈ　ａｃｉｖｔａｔｏｉｎｉｎ　　ｍａｓｔｃｏｙｔｏｓｉｓｗｉ　ｔｈ　ｙＨｅｍｏｎｐｔｒｅａ　ｖｅｎｏ　

ｍ

ａｎａｐｈｙａｌｘｉ［Ｊｓ］Ｃ．ｙｏｔｅｔｍｒｙ　Ｂ　Ｃｌｉ　ｎＣｙｔｏ，２ｍ０１，１８０３）（：１６７－

　１７．５

ｓｌ　Ｅ检测对ｇ敏原过的测范检围宽泛更，ＢＴＡ不仅能　帮助

诊ｓ断ＩＥ阳性ｇ过敏，亦可有能对ｓｇＥｌ检测结果　

［

］Ｒ９ｎａｕｌｅｄ　Ｖ，Ｇｏｕｄｔｅ　Ｖ，ｏｕｔＭｏｎ　Ｆｉａｖｒｅ　Ｃ，ｅｔ　ａ１．Ｃｓａｅ　ｒｅｐｏｔｒ：ｐｅｆｏｉ—

ｐ　ｒｅａｔｉｖｅ　ｉｍｅｍｄｉａｔｅ　ｈｙｐｅｒｓｅｎｓｔｉｉｉｖｙｔ　ｉｎｖｏｖｌｓｅ　ｏｎｌｙ　ａｌｌｒｅｇｙ　ｂｕ　ｔｓｌａｏ

ａｍｓｔｔｏｃｔｙｓｏｉ［ｓ］Ｊ．Ｃａｎ　ＪＡ　ｎａｅｔｓｈ，２０１１５，８５）（：４５６４－５．９　

阴

性非Ｉ即ｇＥ导的过敏诊断有介助。帮ｓＩｇＥ升高只　代表能患者内的一体状态种，并

不代患表者一对　

该定物质产生过反敏应，ｓ即ｌｇ升高Ｅ过与敏反应之　间

［１］Ｆｌ０ａｃｏｎｅ　Ｈ，ＦＺｉｌｉｌｅｋｎ　ｓＤ，ＧｉｂｂｓＢ　．ＦＴｈｅ２　　１ｓｔ　ｃｅｎｕｔｙｒｅ　ｒｎａｉｓｓｎｃｅ　ａ

ｏｆ　ｔｅｈ　ｂａｓｏｐｈｉ？Ｃｌｕｒｅｒｔｎ　ｉｓｎｉｇｈｔｓｉ　ｔｎｏ　ｉｔ　ｓｒｏｌｅ　ｉｎ　ａｌｌｅｒｇｉｃ　ｒｅｓｐｏｓｎｓｅ　

ａ

ｄ　ｎｉｎｎａｔｅ　ｉｍｍｕｎｉｙｔ［Ｊ］Ｅ．ｘｐ　Ｄｒｅｍａｔｏｌ２，０６０，１５（１１）：８５５ — 　

８６４．　

无必联然系。ＢＡＴ结合ｓｌｇＥ检测，对ｓｇｌＥ高升者　的患过敏应反可以明确为ＩＥ依ｇ赖，而引该起患者　ｓＩｇＥ高升过、敏状和症征体的物质即为过原，敏为　患的特异性脱者敏疗治提了重供要依据¨　Ｂ。ＴＡ　

结合ｓｇＥＩ检，测结均果阴为性者，可认以为该物质　不引起是患者过反应敏的敏过原。　综

上述，Ｂ所Ａ对过Ｔ敏原的检测范围比ｓｌｇＥ　检

［

１　１Ｋ］ｎｏｌ　Ｆ．ＥＲｅｑｕｉｅｒｍｅｔｎｓ　ｆｏ　ｒｅｆｅｃｔｉｖｅ　ＩｇＥ　ｃｒｏｓ — ｌｓｉｎｋｉｇ　ｎｏｎｍ　ａｓｔ　ｃｅｌｌｓ

　ａｎｄ　ｂａｓｏｐｈｌｉ［ｓ］Ｊ．Ｍｏｌ　ｕＮｔｒ　ｏＦｏ　Ｒｅｄｓ，２００，６５０（）：６７２￣２０４　

．［１２Ｗ］ｏｏｌｈｉｓｅｒ　Ｍ，ＲＢｏｒｃｋｏｗ　，ＫＭｅｔｃａｌｆｅ　ＤＤ．Ａｃｉｔａｖｔｉｎｏ　ｏｆ　ｈｕｍａｎ　

ｕｍｓｔ　ｃｅｌｌｓ　ｂｙ　ａｇｇｒｅｇａｔｅ　ｄＩｇ　ｔＧｈｒｏｕｇ　ＦｃｈｇａｍａｍＲＩ：ａｄｄｔｉｉｖｅｅ　ｆｅｃｔｓ　

ｏｆ　Ｃ３ａ［］ＪＣｌ．ｉｎ　Ｉｍｍｕｎｏｌ，２０４０，１１（０）２：１７ —２１８．０　［１］Ｓｈ３ｅｅｎ　ＨＣ，ｃＳｈｌｅｉｍｅｒＲ　Ｐ，ｕＫｌｋａ　Ｍ．Ｃｏｄｅｉｎ　ｅｉｎｄｕｅｅｓｈｕｍａ　ｎａｍｓｔ　ｃｅ

ｌｌｃ　ｈｅｍｏｋｎｉ　ｅｎｄａ　ｃｙｔｏｋｉｎｅ　ｐｒｏｄｕｃｔｉｏｎ：ｉｎ

ｖｏｌｖｅｍｅｎｔ　ｏ　ｆＧ —ｐｒｏｔｅｉ　

ｎａ

ｃｉｔｖａｔｉｏ［Ｊｎ］Ａ．ｌｌｅｒ，ｇｙ０２０７，６（２５）：５２３－５８３．［１　］４Ｇｉｂｓｂ　Ｂ，ＦｌＰａｔｈ　ＫＥ，ｏＷｌ　ＨｆＨｅ，ｔ　１．Ｒａｅｇｕｌａｔｉｏｎ　ｏｆ　ｍｅｄｉｔａｏ　ｒｓｅ—

　ｃｅｔｉｒｏｎｉｎ　ｈｕａｍ　ｎｂｓａｏｐｈｉｌｓｂｙ　　ｐ３８　ｍｉｔｏｇｎｅ—ａｃｉｔｖａｅｔｄ　ｐｏｔｒｅｉｎｋｉｎ　ａｓｅ：

　ｐｈｏｓｐｈｏｒｙｌａｔｉｎｏ　ｉｓ　ｓｅｎｓｉｔｖｉｅ　ｔｏ　ｔｈ　ｅｅｆｅｃｔｓ　ｏｆ　ｐｈｓｏｈｐａｔｉｙｌｄｉｎｏｓｉｔｏｌ　３－

测更宽　泛，其不能仅帮助诊ｓ断Ｉｇ阳性Ｅ过敏，亦有　可能对ｓｌｇ检测结果阴性Ｅ非即ｇＩ介导Ｅ的敏过　

诊断有帮助。　参文考：　

［献１Ｈ］ｅ　Ｓ，Ｚｈａｎｇ　，ＨＺｅｎｇ　Ｘ，ｅｔａ　１．Ｓｌｅｆ－ａｍｌｐｉｉｆｃａｔｉｏｎ　ｍｅｃｈａｎｉｓｍｓ　ｏｆ　ｍａｓ　ｔｃｅｌｌ　ａｃｔｖｉｔａｉｏ：ａｎ　ｎｗｅ　ｌｏｏｋｉ　ｎａｌ　ｌｒｅｇｙ［Ｊ］．ＣｕｒｒＭ　ｏｌＭｅｄ　，　２

０１２１，２１（０：）３１９－２１３３９．　

ｋｉｎａｓｅｉ　ｎｈｉｂｉｔｏｍ　ｎｄａ　ｃａｌｉｃｕｍｍｏｂ　ｉｌｉａｚｔｉｏｎ［Ｊ］．Ｊ　Ｌｅｕｋｏｅ　Ｂｉｏｌ，　２

００，２２７（）２：３９１－４００．　

１［５］Ｇｅｒｎｅ　ｚ，ＹＴｉｒｕｏｖｎａｚｉｍ　ａ，ＹＲｕ　Ｇｅ，ｔ　ａ１．ａＢｓｏｈｉｐｌ　ＣＤ２０３　ｌｃｅｖｅｓｌ

　ａｒｅ　ｉｎｃｒｅａｓｄｅ　ａｔ　ｂａｓｅｌｉｎｅ　ａｎｄ　ｃ　ａｎｂ　ｕｅｅ　ｓｔ　ｍｏｏｉｎｔｏｒ　ｏｎａｌｉｚｕｍａｂ　

［２何韶衡．以过］性疾敏发病病制机为基浅础其析助辅断诊段及　临手意床［义Ｊ］．华中临床免疫和变态反杂应志，２０１１，５（１：）一１　

ｔ

ｒａｅｔｍｅｎｔｉ　　ｎｓｕｂｊｅｔｃ　ｓｉｔｗｈ　ｎｕｔ　ｌｌａｅｒｙ

［ｇＪ］Ｉｎ．ｔ　ＡｒｈｃＡｌ　ｌｅｒｙｇ　Ｉｍｍｕ —

ｎ　１ｏ，２０１，１１５４（）４：３８１－３２７．　

（

收稿期日２：０１３ — １００６－）

　１０　

范文三：嗜碱性粒细胞增强记忆性免疫应答

中国肿瘤生物治疗杂志，２００８年８月，１５（４）

［２２］ＣｈｕｎｇＥＪ，Ｓｕｎｇ

ａｎａｌｙｓｉｓ

ｉｎ

ｈｕｍａｎ

ＹＫ，Ｆａｒｏｏｑ

Ｍ，ｅｔ

ａ１．Ｇｅｎｅ

ｂｙ

ｅｘｐｒｅｓｓｉｏｎｅＤＮＡ

ｐｒｏｆｉｌｅ

［２８］Ｓｔｏｆｆ－Ｋｈａｌｉｌｉ

ＭＡ，Ｒｉｖｅｒａ

ａ

ＡＡ，Ｎｅｄｅｌｊｋｏｖｉｃ—Ｋｕｒｅｐａ

Ａ，ｅｔａ１．Ｃａｎ?

ｕｓｉｎｇ

ｈｅｐａｔｏｃｅｌｌｕｌａｒｃａｒｃｉｎｏｍａ

ｍｉｃｒｏａｒｒａｙ

ｃｅｒ?ｓｐｅｃｉｆｉｃｔａｒｇｅｔｉｎｇｏｆｍＲＮＡ

ｔｒａｎｓｌａｔｉｏｎａｌ

ｃｏｎｄｉｔｉｏｎａｌｌｙｒｅｐｌｉｅａｔｉｖｅａｄｅｎｏｖｉｒｕｓ

ＣａｎｃｅｒＲｅｓ

［Ｊ］．ＭｏｌＣｅｌｌｓ，２００２，１４（３）：３８２－３８７．

［２３］Ｂａｕｅｒ

Ｃ。ＤｉｅｓｉｎｇｅｒＩ，ＢｒａｓｓＮ，ｅｔ

ａ１．Ｔｒａｎｓｌａｔｉｏｎｉｎｉｔｉａｔｉｏｎ

ａｍｐｌｉｆｉｅｄ

ｉｎ

ｆａｃｔｏｒ

ｃｏｎｔｒｏｌ［Ｊ］．Ｂｒｅａｓｔ

Ｔｒｅａｔ，２００８，

１０８（１）：４３－５５．

ｅｌＦ－４Ｇｉｓｗｉｔｈ

ｉｍｍｕｎｏｇｅｎｉｃ，ｏｖｅｒｅｘｐｒｅｓｓｅｄ，ａｎｄ

ｌｕｎｇ

ｐａｔｉｅｎｔｓ

［２９］Ｂｙｍｅｓ

Ｋ，ＬｉＢＤ，ＨｏｌｍＮ，ｅｔ

ａ１．Ａｎｏｖｅ｜ｓｕｉｃｉｄｅｇｅｎｅ

ｔｈｅｒａｐｙ

ｉｍ—

ｓｑｕａｍｏｕｓｃｅｌｌｃａｒｃｉｎｏｍａ［Ｊ］．Ｃａｎｃｅｒ，２００１，９２（４）：ｔａｒｇｅｔｉｎｇｔｈｅｏｖｅｒｅｘｐｒｅｓｓｉｏｎｏｆｅｕｋａｒｙｏｔｉ，’ｉｎｉｔｉａｔｉｏｎｉｎ

ａ

ｆａｃｔｏｒ４Ｅ

８２２—８２９．

ｐｒｏｖｅｓｓｕｒｖｉｖａｌ

ｅｕ—

ｒａｔ

ｉ，ｅｒｉｌｏｎｅａｌ

ｃａｒｃｉｎｏｍａｔｏｓｉｓ

ｍｏｄｅｌ［Ｊ］．Ｓｕｒ－

［２４］Ｒａｍｙａ

ｋａｒｙｏｔｉｃ

ＴＮ，ＳｕｒｏｌｉａＮ，ＳｕｒｏｌｉａＡ．１５－ＤｅｏｘｙｓｐｅｒｇｕａｌｉｎｉｎｈｉｂｉｔｓｐｒｏｔｅｉｎｓｙｎｔｈｅｓｉｓｔｈｒｏｕｇｈｅｌＦ２

Ｍｐｈａ

ｇｅｒｙ，２ｆｆ０７，１４２（２）：２７０－２７５．

ｐｈｏｓｐｈｏｒｙｌａｔｉｏｎ［Ｊ］．［３０］ＣｈｕＱＤ．Ｓｕｎ

ｗｉｔｈ

ａｎ

Ｌ，ＬｉＪ，ｅｔ

ａ１．Ｒａｔａｄｅｎｏｃａｒｃｉｎｎｍａｃｅｌｌ

ａ

ｌｉｎｅｉｎｆｅｃｔｅｄ

Ｂｉ，ｘ：ｈｅｍ

Ｊ．２００７。４０１（２）：４１１－４２０．

Ｙ，ＤｅＢｅｎｅｄｅｔｔｉＡ．Ｓｅｌｅｃｔｉｖｅｋｉｌｌｉｎｇｏｆ

ａ

ａｄｅｎｏｖｉｒｏｓ

ｓｕｉｃｉｄｅｇｅｎｅ

ｃａｎｔｉｎｇ

ｎｏｖｅｌ

ｈｅｒｐｅｓ?－ｓｉｍｐｌｅｘｖｉｒｕｓ—?ｔｈｙｍｉｄｉｎｅ

［２５］ＤｅＦａｔｔａＢＪ，Ｌｉ

ｂａｓｅｄ

ｏｎ

ｃａｎｃｅｒｃｅｌｌｓＧｅｎｅ

ｋｉｎａｓｅｃｏｎｓｔｒｕｃｔｄｉｅｓｂｙａｐｏｐｔｏｓｉｓｕｐｏｎｔｒｅａｔｍｅｎｔｗｉｔｈ

ｔｒａｎｓｌａｔｉｏｎａｌｃ，ｏｎｌｒｏｌｏｆｓｕｉｃｉｄｅ

ｇｅｎｅ［Ｊ］．Ｃａｎｃｅｒ

ｇａｎｃｉｃｌｏｖｉｒ［Ｊ］．Ｊ［３１］Ｃｒｅ’ａｎｃｉｅｒ

Ｓｕｒｇ

Ｒｅｓ，２００７，１４３（１）：１８９—１９４．

ａ１．Ｆｉｂｒｏｂｌａｓｔ

ｅｘ

Ｔｈｅｒ，２００２，９（７）：５７３－５７８．Ｌ，ＭｏｒｅｌｌｏＤ，ＭｅｒｃｉｅｒＰ，ｅｔ

ｇｒｏｗｔｈｆａｃｔｏｒ

ｔｒａｎｓ—

［２６］ＤｅＦａｔｔａＲＪ，Ｃｈｅｒｖｅｎａｋ

ＰＹ

ａｐｐｒｏａｃｈ

ｔｈｒｏｕｇｈ

ＲＰ，ＤｅＢｅｎｅｄｅｔｔｉ

Ａ．Ａｏｆ

ａ

ｃａｎｃｅｒ

ｇｅｎｅｔｈｅｒａ?

２ｉｎｔｅｒｎａｌｒｉｂｏｍｍｅ

ａ

ｅｎｔｒｙｓｉｔｅ（ＩＲＥＳ）ａｃｔｉｖｉｔｙ

ｖｉｖｏａｎｄｉｎ

ｔｒａｎｓｌａｔｉｏｎａｌ（?ｏｎｔｒｏｌｓｕｉｃｉｄｅ

ｇｅｎｅ［Ｊ］．ｇｅｎｉｅｍｉｃｅｒｅｖｅａｌｓ

ｓｔｒｉｎｇｅｎｔｔｉｓｓｕｅ—ｓｐｅｃｉｆｉｃ

ｒｅｇｕｌａｔｉｏｎ［Ｊｊ．Ｊ

Ｃｅｌｌ

ＣａｎｃｅｒＧｅｕｅ

Ｔｈｅｒ，２００２，９（６）：５０５－５１２．

ＤＡ，ｅｔａ１．Ｃａｎｃｅｒ—ｓｐｅｌ?ｉｆｉｃ

ｔａｒｇｅ一

ｋｉ一

Ｂｉｏｌ，２０００，１５０（１）：２７５－２８１．

［２７］ＭａｔｈｉｓＪＭ，ＷｉｌｌｉａｍｓＢＪ．Ｓｉｂｌｅｙ

ｔｉｎｇｏｔ’ａｎａｄｅｎｏｖｉｒｕｓｄｅｌｉｖｅｒｅｄｈｅｒｐｅｓｓｉｍｐｌｅｘｖｉｒｕｓ

ｎａｓｅ

ｔｈｙｍｉｄｉｎｅＧｅｎｅ

［收稿日期】２００８一０６一０３［本文编辑］韩丹

［修回日期］２００８－０７—２０

ｓｕｉｃｉｄｅ

ｇｅｎｅ

ｕｓｉｎｇ

ｔｒａｎｓｌａｔｉｏｎａｌ

ｃｏｎｔｒｏｌ［Ｊ］．Ｊ

Ｍｅｄ，

２００６，８（９）：１１０５—１１２０．

气ｅ＾心，譬。气Ｃ代Ｃ气Ｃ噶ｅ噶吐水气心＾心＾—，掣！气ｅ１心“矗，口ｅ气Ｃ‘℃＾心＾心＾瑶，皆巳ｔ４乍ｅ乍ｅｌｅｌ啦＂Ｆ’窜。气ｃ１≈１心／９０ｔ也々ｅ气汜＾心“罐’譬ｅ气世＾也乍ｅＧｃｌ世１心，９０

?科技动态?

嗜碱性粒细胞增强记忆性免疫应答

近年来，人们对嗜碱性粒细胞免疫功能的认识逐渐加深。来自德国雷根斯馒大学医院的Ｍａｃｋ等学者在２００８年７月的

Ｎａｔｕｒｅ

Ｉｍｍｕｎｏｌｏｇｙ杂志上发表的文章表明，再次免疫应答过程中的嗜碱性粒细胞能通过表面ＩｇＥ结合抗原并通过分泌ＩＬ－４和

ＩＬ－６等细胞因子增强记忆性Ｂ细胞免疫应答。

嗜碱性粒细胞足一种数量很少的粒细胞，在人和小鼠的外周血白细胞中的比例为１％以下。以往对该细胞的研究卡要集中在致敏原和某些寄生虫感染引发的过敏反应，对其免疫调节功能了解很少。现自．研究表明，嗜碱性粒细胞可通过表面高亲和力的ＩｇＥ受体ＦｃｅＲｌ结合初次应答中产牛的抗原特异性ＩｇＥ，当相同抗原冉次进入机体后，结合了ｌｇＥ的嗜碱性粒细胞就能通过表面结合的ｌｇＥ迅速结合抗原并活化，产生大量ｌＬ４和ＩＩ。＿６。上述两种细胞闪子具有促进体液免疫应答的作用。因此，作者推测嗜碱性粒细胞在再次免疫应答中的活化町能促进记忆性Ｂ细胞体液免疫应答的作用。

实验首先采用了别藻蓝蛋白（ＡＰＣ）作为抗原免疫小鼠，数周后用ＡＰＣ进行再刺激，发现免疫后的小鼠体内长期存在能够通过表面ＩｇＥ结合ＡＰＣ的嗜碱性粒细胞。再次应答中该群嗜碱性粒细胞结合ＡＰＣ抗原后能够迅速活化并成为脾脏和骨髓细胞中ＩＬ－４和ＩＬ－６的主要分泌细胞。嗜碱性粒细胞的这一活化过程依赖Ｆｃ受体＾ｙ链。再次应答前采用抗体腹腔注射清除体内嗜碱性粒细胞后，再次应答所产生的抗原特异性ＩｇＧｌ和ｌｇＧ２ａ分别减少５０％和６０％一８０％，同时抗原特异性Ｂ细胞和浆细胞数也显著下降。如果将经过免疫的小鼠脾脏或骨髓细胞去除浆细胞后过继到未经免疫的小鼠体内，该受体小鼠在ＡＰＣ抗原刺激下可产生一定水平的特异性抗体；如果将脾脏或骨髓细胞中的嗜碱性粒细胞清除后再进行过继，则受体小鼠在ＡＰＣ刺激下产生的特异性抗体显著减少。作者通过体外实验发现，在活化的Ｃ１ＭＴ细胞存在下，活化的嗜碱性粒细胞能够促进Ｂ细胞增殖，并分泌ＩｇＧ和ＩｇＭ抗体。此外，嗜碱性粒细胞通过分泌ＩＬ－６促进活化的ＣＤ４Ｔ细胞分泌ＩＬ－４、ＩＬ－５、ＩＬ一１０、ＩＬ一１３，促进其表达Ｇａｔａ３，下调ＩＦＮ一１和ＩＬ－２表达，成为促进体液免疫应答的Ｔｈ２。

该研究表明，嗜碱性粒细胞除ｒ在某些过敏反应中发挥重要作用外，还可能具有很多以前没有认识到的功能，有待进一步的探索。

［姚雨石摘译，郭振红审阅．Ｄｅｎｚｅｌ

Ａ，ＭａｕｓＵＡ，ＲｏｄｒｉｇｕｅｚＧｏｍｅｚＭ，ｅｔａ１．Ｎａｔ

Ｉｍｍｕｎｏｌ，２００８，９（７）：７３３－７４２］

万方数据

范文四：调节人嗜碱性粒细胞脱颗粒

See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/262189657 Modulation Of Human Basophil Degranulation By Geranylgeranyl Compounds

Article in Allergology International · May 2014

DOI: 10.2332/allergolint.13-LE-0637 · Source: PubMed

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Dear Editor

Modulation of Human Basophil Degranulation by Geranylgeranyl

Compounds

Recent experimental studies have shown that the ba-sophil is critical for a subtype of anaphylaxis or IgE-mediated very late-phase skin inflammation. 1Motility and activation of basophils are known to be regulated by various endogenous and ! or exogenous sub-stances. The panel of known such basophil-directed molecules is expanding. One important candidate may be geranylgeranyl compounds, which were in-itially demonstrated to be protectors of the gastric mucosa. 2These compounds have also demonstrated protective actions in situations that are often hazard-ous to the host. In rodent studies, geranylgeranylace-tone (GGA)suppressed the development of several inflammatory reactions and enhanced tissue regen-eration in vivo . 2,3However, the effects of GGA on al-lergic effectors and immunologic reactions have not been fully clarified.

In this study, we assessed the pharmacological ac-tions of GGA and related compounds on basophil de-granulation, detected as release of histamine. Baso-phils were obtained from non allergic volunteers by dextran sedimentation of whole blood. Cells were preincubated with GGA (Wako Pure Chemicals, Osaka, Japan) for 15min at 37 , washed and then stimulated with a secretagogue for 45min. 4

Degranulation of basophils by polyclonal anti-IgE antibody (MBL, Nagoya, Japan ) and by phorbol myristate acetate (PMA ) (Sigma, St. Louis, MO, USA) was significantly enhanced by preincubation of cells for 15min with GGA at 1.4or 2.7mM (Fig.1a). Similar results were observed for highly pure baso-phils (purity>95%;prepared by Percoll gradient cen-trifugation followed by negative MACS selection), in-dicating that GGA acts directly on basophils. On the other hand, GGA showed no clear effect on basophil degranulation by a chemokine, monocyte chemoat-tractant protein (MCP)-1or Ca ionophore A23187. As shown in Figure 1b, up to 15min of incubation of ba-sophils with GGA alone at 2.7mM did not induce re-lease of histamine. However, 30min or longer incuba-tion resulted in higher, 15to 20%histamine release, suggesting that GGA at this concentration might damage basophils in a time-dependent manner. The extent of enhancement of IgE-mediated basophil de-granulation by GGA was mild compared to that by IL-3, and GGA did not show additive augmentation of histamine release by IL-3-treated basophils (Fig.1c). As shown in Figure 1d, another geranylgeranyl com-pound, geranylgeraniol (Sigma),also upregulated ba-sophil histamine release evoked by anti-IgE antibody

or PMA. On the other hand, compounds having

smaller structures, such as geranylacetone and farne-sol, showed no effect on basophil degranulation (datanot shown). Statins inhibit intracellular geranylger-anylation, resulting in suppression of the activation profiles of inflammatory cells, 5-7and basophil de-granulation in response to anti-IgE antibody or PMA was significantly suppressed by preincubation with simvastatin at 50μM(Fig.1e).

Geranylgeranyl compounds are reported to be in-volved in intracellular signal cascades in various cells, including mast cell activation evoked by IgE crosslinkage. 5-7Our present finding that exogenously added GGA can enhance basophil activation suggests that GGA enters basophils and then behaves as a sub-strate in the cell activation pathway. Simvastatin, which can inhibit intracellular geranylgeranylation, suppressed basophil degranulation triggered by anti-IgE antibody and PMA, but not A23187. This finding coincides with our results that GGA augmented baso-phil degranulation evoked by anti-IgE antibody and PMA, but not A23187or MCP-1, suggesting that pro-tein kinase C or related molecule(s)may be the tar-get of GGA. It appears that geranyl and farnesyl com-pounds are not involved in the above pathway in ba-sophils.

GGA’s various novel actions are being unveiled through recent experimental approaches. Mostly based on murine studies, this compound is able to suppress vicious inflammatory disorders of the skin or visceral organs, including pulmonary inflammation induced by gefitinib, an inhibitor of epidermal growth factor receptor-mediated signals. 3It is thought that one of main in vivo effects of GGA is induction of tissue-stabilizing heat shock proteins. 2,3In vivo stud-ies have so far tested GGA at μMto mM concentra-tions and have found increases in those proteins and changes in cell fate. 8,9Our present findings suggest that GGA at relatively high concentrations can also exert acute effects on cellular functions and enhance the activation of basophils evoked by certain secre-tagogues. Although the in vivo significance of our findings and the whole aspect of the biologic actions of GGA remain unclear, elucidation of the precise roles of this compound in allergies and other tissue-damaging disorders is of special interest in light of its characteristic host-protecting properties.

ACKNOWLEDGEMENTS

The authors thank Ms. Sayaka Igarashi for her excel-lent technical help.

Yuko Nakase 1, Masao Yamaguchi 1, Naoya Sugimoto 1, Maho Suzukawa 2,

Hidenori Arai 1, Hiroyuki Nagase 1and Ken Ohta 1,2

Allergology International. 2014;63(Suppl1):49-51

DOI:10.2332! allergolint.13-LE-0637

Nakase Y et al.

Allergology International Vol 63, Suppl 1, 2014www.jsaweb.jp !

Fi g . 1 Mod u lation of b asophil histamine release b y geranylgeranyl and related compou nds. (a ) Basophil preparations w ere preinc ub ated w ith and w itho u t GGA and then stimu lated w ith variou s secretagogu es. GGA at 1.4 and 2.7 mM corresponds to 0.5 and 1 μl/ml, respectively. Histamine release w as expressed as a percentage of the total cellu lar histamine after sub tracting spontaneo u s release (u s u ally <5%). data="" are="" the="" mean="" ±="" sem="" of="" three="" to="" six="" separate="" experiments.="" *p="" ≤="" 0.05,="" versu="" s="" corre-sponding="" valu="" es="" of="" cells="" not="" preincub="" ated="" w="" ith="" gga.="" (b="" )="" baseline="" histamine="" release="" b="" y="" b="" asophils="" after="" treatment="" w="" ith="" gga.="" cells="" w="" ere="" preincub="" ated="" w="" ith="" gga="" at="" 1="" μl/ml="" for="" the="" indicated="" times,="" w="" ashed="" and="" then="" incub="" ated="" w="" itho="" u="" t="" any="" secretagogu="" e="" for="" 45="" min.="" data="" show="" n="" are="" representative="" of="" three="" separate="" experiments="" that="" generated="" similar="" resu="" lts.="" (c="" )="" priming="" effects="" of="" gga="" and="" il-3="" on="" b="" asophil="" degranu="" lation.="" cells="" w="" ere="" preincub="" ated="" w="" ith="" and="" w="" itho="" u="" t="" gga="" for="" 15="" min,="" w="" ashed="" and="" then="" incub="" ated="" w="" ith="" and="" w="" itho="" u="" t="" il-3="" b="" efore="" stimu="" lation="" w="" ith="" anti-ige="" antib="" ody.="" data="" are="" the="" mean="" ±="" sem="" (n="3)." *p="">< 0.05="" versu="" s="" corresponding="" val="" u="" e="" of="" cells="" not="" preincub="" ated="" w="" ith="" gga.="" p="">< 0.05="" versu="" s="" corresponding="" valu="" e="" of="" il-3-u="" ntreated="" cells.="" (d="" )="" effect="" of="" geranyl-geraniol="" on="" b="" asophil="" histamine="" release.="" the="" indicated="" concentration="" of="" this="" compou="" nd="" (0.5="" μl/ml,="" 1.5="" mm)="" did="" not="" indu="" ce="" non-specifi="" c="" histamine="" release.="" data="" are="" the="" mean="" ±="" sem="" (n="3)." *p="">< 0.05="" versu="" s="" corresponding="" valu="" e="" of="" cells="" not="" preincub="" ated="" w="" ith="" geranylgeraniol.="" (e="" )="" simvastatin="" su="" ppressed="" b="" asophil="" degranu="" lation.="" basophils="" w="" ere="" preincub="" ated="" w="" ith="" and="" w="" itho="" u="" t="" simvas-tatin="" for="" 15="" min="" at="" 37?c,="" w="" ashed="" and="" then="" stimu="" lated="" w="" ith="" anti-ige="" antib="" ody="" or="" pma="" for="" 45="" min.="" data="" are="" the="" mean="" ±="" sem="" (n="4)." *p="">< 0.05,="" versu="" s="" corresponding="" valu="" e="" of="" cells="" u="" ntreated="" w="" ith="">

100

a 80

6040200

10080604020

GGA (mM) - 2.7 - 2.7 IL-3 (pM) - - 300 300 a nti-IgE (Pg/ml) 1.4 14

1.4 14

1.4 14 1.4 14

1.414401000.10.210100PMA (ng/ml)

Pretreatment with GGAGGA (-)

GGA 1.4 mMGGA 2.7 mM

A23187 (Pg/ml)anti-IgE (Pg/ml)MCP-1 (nM)H i s t a m i n e r e l e a s e (%)

c H i s t a m i n e r e l e a s e (%) 80604020

100806040200

d H i s t a m i n e r e l e a s e (%) 30

1.4141000.2MCP-1(nM)A23187(Pg/ml)

10anti-IgE (Pg/ml)

PMA

(ng/ml)100Statin (PM) -50

-50

1.4 141.4 1410 100anti-IgE (Pg/ml)

PMA (ng/ml)

10 100515Pretreatment with GGA (min)

Pretreatment with

geranylgeraniol 30(-)1.5 mM

60120b B a s e l i n e h i s t a m i n e r e l e a s e (%)

GGA Modulates Basophil Activation

Allergology International Vol 63, Suppl 1, 2014www.jsaweb.jp !

1Division

of Respiratory Medicine and Allergology,

Department of Medicine, Teikyo University School of Medicine and 2National Hospital Organization Tokyo National Hospital, Tokyo, Japan Email:myama@med.teikyo?u.ac.jp

Conflict of interest:No potential conflict of interest was disclosed.

REFERENCES

1. H, Mukai K, Obata K, Tsujimura Y, Wada T.

Nonredundant roles of basophils in immunity. Annu Rev Immunol 2011; 29:45-69.

2. Ishihara T, Suemasu S, Asasno T, Tanaka K, Mizushima T. Stimulation of gastric ulcer healing by heat shock pro-tein 70. Biochem Pharmacol 2011; 82:728-36.

3. T, Tanaka K, Hoshino T, Azuma A, Mizushima T. Suppression of expression of heat shock protein 70by ge-fitinib and its contribution to pulmonary fibrosis. PLoS One 2011; 6:e27296.

4. Koketsu R, Yamaguchi M, Suzukawa M et al . Pretreat-ment with low levels of Fc εRI-crosslinking stimulation en-hances basophil mediator release. Int Arch Allergy Immu-nol 2013; 161:S23-31.

5. Fujimoto M, Oka T, Murata T, Hori M, Ozaki H. Fluvasta-inhibits mast cell degranulation without changing the cytoplasmic Ca 2+level. Eur J Pharmacol 2009; 602:432-8.6. Majlesi Y, Samorapoompichit P, Hauswirth AW et al . Cerivastatin and atorvastatin inhibit IL-3-dependent differ-entiation and IgE-mediated histamine release in human basophils and downmodulate expression of the basophil-activation antigen CD203c ! E-NPP3. J Leukoc Biol 2003; 73:107-17.

7. Graham TE, Pfeiffer JR, Lee RJ et al . MEK and ERK acti-vation in ras-disabled RBL-2H3mast cells and novel roles for geranylgeranylated and farnesylated proteins in Fc εRI -mediated signaling. J Immunol 1998; 161:6733-44.

8. Endo S, Hiramatsu N, Hayakawa K et al . Geranylgerany-lacetone, an inducer of the 70-kDa heat shock protein (HSP70),elicits unfolded protein response and coordi-nates cellular fate independently of HSP70. Mol Pharma-col 2007; 72:1337-48.

9. Nanke Y, Kawamoto M, Yago T, Chiba J, Yamanaka H, Kotake S. Geranylgeranylacetone, a non-toxic inducer of shock protein, induces cell death in fibroblast-like synoviocytes from patients with rheumatoid arthritis. Mod Rheumatol 2009; 19:379-83.

范文五：嗜碱性粒细胞百分比偏低的平衡方法

嗜碱性粒细胞百分比偏低的平衡方法

我们可能对于嗜碱性粒细胞百分比偏低还不太了解吧，这是反映我们正常身体机能的一项指标，颈动脉彩超正常值可以详细的客观的反应我们身体某一方面的情况变化，通过对嗜碱性粒细胞百分比的了解，我们可以及时有效的对我们的身体做出调整，补充身体没缺乏的营养物质，如果有疾病就要及时去医院就诊，如何才能平衡嗜碱性粒细胞百分比偏低呢,下面就让我们一起来了解一下。

治疗方法:

1.如果是感冒会引起嗜酸性粒细胞百分比升高，主要是病毒性感染导致，如果不严重可以多喝水，注意休息，可以痊愈，如果严重可以口服一些中药制剂，如感冒清热颗粒等。还有大便出血现象是经常性的，还是偶尔的，如果经常性的你先查一下大便情况，一般有痔疮也会导致大便出血，要经常保证大便通畅，避免便秘。

2.嗜酸性粒细胞偏高一般提示有过敏或蛔虫感染等情况，要找出病因彻底治愈病根才能改善嗜酸性粒细胞的比值。如果有的话，可以用抗过敏的药物调节如扑尔敏，或赛庚啶等;或化验大便看是否存在蛔虫感染，有的话打虫治疗如，安乐士，肠虫清等，治愈好原发病的话，嗜酸性粒细胞比值会降至正常。

3治疗使用抗组胺类药物(如氯雷他定片)和维生素C片，钙剂，激素等外，平时的生活饮食卫生和个人卫生也是非常重要的，注意饮食，避免诱因，避免接触花粉，粉尘等。过敏性鼻炎的发病与饮食有—————————————————————————————————————————————————————

一定的关系，某些食物可能是诱因。例如鱼虾海鲜，含有人工色素、防腐剂、酵母菌等人工添加剂的罐头、腌腊食品、饮料等都可诱发，还应忌酸辣。保持健康心态，提高身体抵抗力。

以上内容为我们介绍了如何平衡嗜碱性粒细胞百分比偏低，通过以上内容，当我们自身再出现嗜碱性粒细胞百分比偏低的情况，就可以运用以上的方法进行治疗，就可以免去四处求医问诊的困难，尽快恢复身体健康。

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