中华血液学杂志
中華血液學雜誌
중화혈액학잡지
Chinese Journal of Hematology
2011年
8期
525-528
,共4页
张弦%张艳玲%王建玲%童春容%蔡鹏%刘红星%王静波%曹星玉%殷宇明%吴彤
張絃%張豔玲%王建玲%童春容%蔡鵬%劉紅星%王靜波%曹星玉%慇宇明%吳彤
장현%장염령%왕건령%동춘용%채붕%류홍성%왕정파%조성옥%은우명%오동
受体,免疫球蛋白样%预后%移植物抗宿主病%复发
受體,免疫毬蛋白樣%預後%移植物抗宿主病%複髮
수체,면역구단백양%예후%이식물항숙주병%복발
Immunoglobulin-like receptor%Prognosis%Graft-versus-host disease%Relapse
目的 分别探讨NK细胞中抑制性和激活性免疫球蛋白样受体(KIR)在亲缘半相合造血干细胞移植(HSCT)中的作用.方法 检测47例亲缘半相合HSCT中的供者KIR基因型和患者HLA-C基因型,随访移植后2年总生存率、Ⅲ～Ⅳ度急性移植物抗宿主病(GVHD)发生率和复发率.结果 ①按供受者抑制性KIR与其配体HLA-C是否匹配分为两组,匹配组的2年总生存率明显高于不匹配组[分别为(87.5±8.3)%和(54.5±9.0)%,P=0.03];复发率明显降低[分别为0和(25.4±9.5)%,P=0.05].将病例分为髓系白血病和淋巴细胞白血病,其中30例髓系白血病患者中匹配组复发率明显低于不匹配组[分别为0和(35.0±14.4)%,P=0.04].其他项目差异无统计学意义.②常见的激活性KIR主要包括3个:KIR2DS1、KIR2DS2、KIR2DS3.分别按其供者是否表达进行单因素分析,其中KIR2DS1(+)组Ⅲ～Ⅳ度急性GVHD发生率比KITR2DS1(-)组低(分别为13%和28%,P＞0.05);KIR2DS2(+)组复发率低于KIR2DS2(-)组[分别为0和(17.3±7.1)%,P＞0.05];KIR2DS3(+)组Ⅲ～Ⅳ度急性GVHD发生率低于KIR2DS3(-)组(分别为11%和26%,P＞0.05);其他无明显差异.结论 ①亲缘半相合HSCT中,供者抑制性KIR与患者HLA-C匹配组较不匹配组总体生存率明显升高,复发率明显降低.特别在髓系白血病中,复发率明显降低.②对于激活性KIR受体中KIR2DS1或KIR2DS3的表达,可能降低急性重度GVHD的发生率;而KIR2DS2(+)组表达,可能降低复发率.
目的 分彆探討NK細胞中抑製性和激活性免疫毬蛋白樣受體(KIR)在親緣半相閤造血榦細胞移植(HSCT)中的作用.方法 檢測47例親緣半相閤HSCT中的供者KIR基因型和患者HLA-C基因型,隨訪移植後2年總生存率、Ⅲ～Ⅳ度急性移植物抗宿主病(GVHD)髮生率和複髮率.結果 ①按供受者抑製性KIR與其配體HLA-C是否匹配分為兩組,匹配組的2年總生存率明顯高于不匹配組[分彆為(87.5±8.3)%和(54.5±9.0)%,P=0.03];複髮率明顯降低[分彆為0和(25.4±9.5)%,P=0.05].將病例分為髓繫白血病和淋巴細胞白血病,其中30例髓繫白血病患者中匹配組複髮率明顯低于不匹配組[分彆為0和(35.0±14.4)%,P=0.04].其他項目差異無統計學意義.②常見的激活性KIR主要包括3箇:KIR2DS1、KIR2DS2、KIR2DS3.分彆按其供者是否錶達進行單因素分析,其中KIR2DS1(+)組Ⅲ～Ⅳ度急性GVHD髮生率比KITR2DS1(-)組低(分彆為13%和28%,P＞0.05);KIR2DS2(+)組複髮率低于KIR2DS2(-)組[分彆為0和(17.3±7.1)%,P＞0.05];KIR2DS3(+)組Ⅲ～Ⅳ度急性GVHD髮生率低于KIR2DS3(-)組(分彆為11%和26%,P＞0.05);其他無明顯差異.結論 ①親緣半相閤HSCT中,供者抑製性KIR與患者HLA-C匹配組較不匹配組總體生存率明顯升高,複髮率明顯降低.特彆在髓繫白血病中,複髮率明顯降低.②對于激活性KIR受體中KIR2DS1或KIR2DS3的錶達,可能降低急性重度GVHD的髮生率;而KIR2DS2(+)組錶達,可能降低複髮率.
목적 분별탐토NK세포중억제성화격활성면역구단백양수체(KIR)재친연반상합조혈간세포이식(HSCT)중적작용.방법 검측47례친연반상합HSCT중적공자KIR기인형화환자HLA-C기인형,수방이식후2년총생존솔、Ⅲ～Ⅳ도급성이식물항숙주병(GVHD)발생솔화복발솔.결과 ①안공수자억제성KIR여기배체HLA-C시부필배분위량조,필배조적2년총생존솔명현고우불필배조[분별위(87.5±8.3)%화(54.5±9.0)%,P=0.03];복발솔명현강저[분별위0화(25.4±9.5)%,P=0.05].장병례분위수계백혈병화림파세포백혈병,기중30례수계백혈병환자중필배조복발솔명현저우불필배조[분별위0화(35.0±14.4)%,P=0.04].기타항목차이무통계학의의.②상견적격활성KIR주요포괄3개:KIR2DS1、KIR2DS2、KIR2DS3.분별안기공자시부표체진행단인소분석,기중KIR2DS1(+)조Ⅲ～Ⅳ도급성GVHD발생솔비KITR2DS1(-)조저(분별위13%화28%,P＞0.05);KIR2DS2(+)조복발솔저우KIR2DS2(-)조[분별위0화(17.3±7.1)%,P＞0.05];KIR2DS3(+)조Ⅲ～Ⅳ도급성GVHD발생솔저우KIR2DS3(-)조(분별위11%화26%,P＞0.05);기타무명현차이.결론 ①친연반상합HSCT중,공자억제성KIR여환자HLA-C필배조교불필배조총체생존솔명현승고,복발솔명현강저.특별재수계백혈병중,복발솔명현강저.②대우격활성KIR수체중KIR2DS1혹KIR2DS3적표체,가능강저급성중도GVHD적발생솔;이KIR2DS2(+)조표체,가능강저복발솔.
Objective To investigate the effect of inhibitory and activating KIRs on a cohort of Chinese leukemia patients who received haplo-identical hematopoietic stem cell transplantation (HSCT).Methods Donor' s inhibitory and activating KIRs and recipient' s HLA-C from 47 cases who received haplo-identical HSCT were tested by PCR-SSP.2 year overall survival ( OS), incidence of severe ( grade Ⅲ to Ⅳ )acute GVHD (aGVHD) and relapse rate(RR) were analyzed.Results ①According to Matched (M) vs Mis-Matched( MM ) between donor' s inhibitory KIR and recipient' s HLA-C1/C2 subgroup, 2 year OS rate in M group[(87.5 ±8.3)%]was significantly higher than that in MM group (54.5 ±9.0)%, (P=0.03).Lower incidence of relapse rate was seen in M group than in M/MM groups[0 vs (25.4 ±9.5)%, P =0.05].In 30 cases of myeloid leukemia patients, there was lower RR in M group than in MM groups[0 vs (35.0 ± 14.4) % ,P = 0.04].②According to the 3 activating KIR genes: KIR2DSI/KIR2DS2/KIR2DS3,lower incidence of grade Ⅲ - Ⅳ aGVHD was seen in KIR2DS1 ( + ) group than in KIR2DS1 ( - ) group ( 13% vs 28%, respectively, P＞0.05); and so was done in KIR2DS3( + ) group( 11% vs 26%, respectively, P＞0.05).The RR was lower in KIR2DS2( + ) group[0% vs (17.3 +7.1)%, respectively, P＞0.05].Conclusions In our haplo-identical HSCT setting, match between donor' s inhibitory KIR and recipient's HLA-C can significantly reduce the incidence of relapse rate and improve OS.Although lower incidences of severe aGVHD are noted in the donors with KIR2DS1 ( + ) or KIR2DS3 ( + ), and lower relapse rate is noted in the donors with KIR2DS2( + ) but without statistic difference, no remarkable effects of activating KIRs on OS have been found in our relatively small clinical series.
