滤泡辅助性T细胞及半乳糖缺乏的IgAn 1在儿童过敏性紫癜发病机制中的意义n

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目的:探讨滤泡辅助性T(follicular helper T,Tfh)细胞和半乳糖缺乏的IgAn 1(galactose-deficient IgAn 1,Gd-IgAn 1)在儿童过敏性紫癜(Henoch-Sch?nlein purpura,HSP)及紫癜性肾炎(Henoch-Sch?nlein purpura nephritis,HSPN)发生发展中的作用及二者之间相关性。n 方法:选取初发HSP患儿62例,根据是否合并肾脏损害分为HSP组(32例)和紫癜性肾炎(HSPN)组(30例)。另选取20例门诊体检儿童作为健康对照组。采用流式细胞术检测外周血中Tfh细胞(CD4n +CXCR5n +PD-1n +)比例。采用免疫比浊法检测血清IgA表达水平、采用ELISA法检测血清Gd-IgAn 1表达水平。n 结果:(1)HSP组和HSPN组患儿外周血中Tfh细胞比例、血清Gd-IgAn 1的表达水平较健康对照组显著升高(n P<0.01),HSPN组较HSP组明显增高(n P<0.05)。(2)HSPN组中,肾脏病理Ⅲ级及以上患儿、大量蛋白尿患儿外周血Tfh细胞比例、血清Gd-IgAn 1表达水平分别较肾脏病理Ⅲ级以下患儿、非大量蛋白尿患儿明显升高(n P<0.01)。(3)健康对照组儿童外周血Tfh细胞比例与血清Gd-IgAn 1水平、血清IgA及Gd-IgAn 1水平均呈正相关关系(n P0.05)。n 结论:Tfh细胞过度活化、血清Gd-IgAn 1水平增高可能是HSP/HSPN发病机制之一,二者升高的程度与疾病的活动度及严重程度可能相关。Tfh细胞可能导致Gd-IgAn 1生成增加的机制有待进一步研究。n “,”Objective:To investigate the role of follicular helper T(Tfh) cells and galactose deficiency IgAn 1(Gd-IgAn 1) in the children that were suffering from Henoch-Sch?nlein purpura(HSP) and Henoch-Sch?nlein purpura nephritis(HSPN)and the correlation between them.n Methods:According to the presence or absence of renal injury, 62 children with HSP were divided into HSP group with 32 children and HSPN group with 30 children.Twenty children who underwent physical examination at outpatients were known as the healthy control group.Flow cytometry was used to measure the proportion of Tfh(CD4n + CXCR5n + PD-1n + ) in peripheral blood.Immunoturbidimetry and ELISA were used to measure the serum levels of IgAn 1 and Gd-IgAn 1 respectively.n Results:(1) The proportion of Tfh cells in peripheral blood and the serum levels of Gd-IgAn 1 in both HSP group and HSPN group had significantly increased than those in healthy control group(n P<0.01). Compared result of the HSPN group with HSP group, the proportion of Tfh cells in peripheral blood and the serum levels of Gd-IgAn 1 in HSPN group were higher than that in HSP group(n P<0.05). (2) In the HSPN group, the proportion of peripheral blood Tfh cells and the serum levels of Gd-IgAn 1 in group of renal pathology ≥ grade Ⅲ and heavy proteinuria were significantly elevated compared with group of renal pathology < grade Ⅲ and non-heavy proteinuria(<0.01). (3) In the healthy control group, the serum levels of Gd-IgA n 1 was positively correlated with the proportion of Tfh cells in peripheral blood and the serum levels of Gd-IgAn 1(n P0.05).n Conclusion:The excessive activation of Tfh cells and the serum levels of Gd-IgAn 1 may be one of the pathogenesis of HSP/HSPN, the degree of increment of the two factors may be related to the activity and severity of the disease.The mechanism of Tfh cells potentially leading to an increase of Gd-IgAn 1 production requires further study.n
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