CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Killer Cell Immunoglobulin-like Receptors (KIR) and Human Leucocyte Antigen C (HLA-C) Increase the Risk of Long-Term Chronic Liver Graft Rejection.
Killer Cell Immunoglobulin-like Receptors (KIR) and Human Leucocyte Antigen C (HLA-C) Increase the Risk of Long-Term Chronic Liver Graft Rejection.
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慢性肝脏排斥反应（CR）是一种复杂的临床情况，因为许多患者对增加免疫抑制治疗无应答。杀伤细胞免疫球蛋白样受体/人白细胞抗原I类（KIR/HLA-I）相互作用可用于预测自然杀伤（NK）细胞异体反应性，并影响肝移植物急性排斥反应；但其在肝移植物CR中的意义仍有争议。采用序列特异性寡核苷酸聚合酶链式反应（PCR-SSO）方法，研究513例肝移植患者的KIR和HLA基因型。分析并比较总体移植患者中发生CR者（n=35）和无慢性排斥者（NCR，n=478）的KIR、人白细胞抗原C（HLA-C）基因型、KIR基因错配以及KIR/HLA配体。与NCR组相比，受者激活性KIR（aKIR）基因rKIR2DS2+和rKIR2DS3+与CR增加相关（p分别为0.013和0.038）。
受者抑制性KIR基因rKIR2DL2+者CR率显著高于无该基因者（9.1%比3.7%，p=0.020）。KIR2DL3也显著增加CR（13.1%比5.2%，p=0.008），但对NCR无影响。HLA-I错配（MM）中也观察到CR。供者缺乏HLA-C2配体（dC2−）者CR增加（与存在该配体者相比13.1%比5.6%，p=0.018）。rKIR2DL3+/dC1−（p=0.015）、rKIR2DS4/dC1−（p=0.014）及rKIR2DL3+/rKIR2DS4+/dC1−（p=0.006）组合与CR显著增加相关。移植后5–10年，rKIR2DS1+/rKIR2DS4+/dC1−患者长期生存显著较低。
本研究显示，受者KIR/供者HLA-C组合及aKIR基因间错配会增加CR；KIR2DS1+/C1配体及KIR2DS4+/C1配体会影响移植物长期生存。
Chronic liver rejection (CR) represents a complex clinical situation because many patients do not respond to increased immunosuppression. Killer cell immunoglobulin-like receptors/Class I Human Leukocyte Antigens (KIR/HLA-I) interactions allow for predicting Natural Killer (NK) cell alloreactivity and influence the acute rejection of liver allograft.
However, its meaning in CR liver graft remains controversial. KIR and HLA genotypes were studied in 513 liver transplants using sequence-specific oligonucleotides (PCR-SSO) methods. KIRs, human leucocyte antigen C (HLA-C) genotypes, KIR gene mismatches, and the KIR/HLA-ligand were analyzed and compared in overall transplants with CR (n = 35) and no-chronic rejection (NCR = 478). Activating KIR (aKIR) genes in recipients (rKIR2DS2 + and rKIR2DS3 + ) increased CR compared with NCR groups ( p = 0. 013 and p = 0. 038). The inhibitory KIR (iKIR) genes in recipients rKIR2DL2 + significantly increased the CR rate compared with their absence (9.
1% vs. 3. 7%, p = 0. 020). KIR2DL3 significantly increases CR (13. 1% vs. 5. 2%; p = 0. 008). There was no influence on NCR. CR was observed in HLA-I mismatches (MM). The absence of donor (d) HLA-C2 ligand (dC2 - ) ligand increases CR concerning their presence (13. 1% vs. 5.
6%; p = 0. 018). A significant increase of CR was observed in rKIR2DL3 + /dC1 - ( p = 0. 015), rKIR2DS4/dC1 - ( p = 0. 014) and rKIR2DL3 + /rKIR2DS4 + /dC1 - ( p = 0. 006). Long-term patient survival was significantly lower in rKIR2DS1 + rKIR2DS4 + /dC1 - at 5-10 years post-transplant.
This study shows the influence of rKIR/dHLA-C combinations and aKIR gene-gene mismatches in increasing CR and KIR2DS1 + /C1-ligands and the influence of KIR2DS4 + /C1-ligands in long-term graft survival.
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