Lung Research, Hanson Institute and Department of Thoracic Medicine, Royal Adelaide Hospital, Australia.
Clin Exp Immunol. 2013 Jul;173(1):150-60. doi: 10.1111/cei.12081.
Bronchiolitis obliterans syndrome (BOS) is associated with lack of immunosuppression of T cell proinflammatory cytokines and increased T cell granzyme B. Repeated antigen-driven proliferation down-regulates T cell CD28. We hypothesized that down-regulation of CD28 and up-regulation of alternate co-stimulatory molecules (CD134, CD137, CD152 and CD154) on T cells may be associated with BOS. Co-stimulatory molecules, granzyme B, perforin and intracellular cytokines were measured by flow cytometry on T cells from stable lung transplant patients (n = 38), patients with BOS (n = 20) and healthy controls (n = 10). There was a significant increase in the percentage of CD4/28(null) and CD8/28(null) T cells producing granzyme B, interferon (IFN)-γ and tumour necrosis factor (TNF)-α in BOS compared with stable patients. Down-regulation of CD28 was associated with steroid resistance and up-regulation of CD134, CD137, CD152 and CD154 on CD4(+) T cells and CD137 and CD152 on CD8(+) T cells. There was a significant correlation between increased CD28(null) /CD137 T cells producing IFN-γ, TNF-α with BOS grade (r = 0·861, P < 0·001 for CD28(null) /CD137 IFN-γ/CD8) and time post-transplant (r = 0·698, P < 0·001 for CD28(null) /CD137 IFN-γ/CD8). BOS is associated with down-regulation of CD28 and up-regulation of alternate co-stimulatory molecules on steroid-resistant peripheral blood proinflammatory CD4(+) and CD8(+) T cells. Therapeutic targeting of alternate co-stimulatory molecules on peripheral blood CD28(null) T cells and monitoring response using these assays may help in the management of patients with BOS.
闭塞性细支气管炎综合征(BOS)与 T 细胞前炎性细胞因子的免疫抑制缺乏和 T 细胞颗粒酶 B 的增加有关。反复的抗原驱动增殖会下调 T 细胞 CD28。我们假设 T 细胞上 CD28 的下调和替代共刺激分子(CD134、CD137、CD152 和 CD154)的上调可能与 BOS 有关。通过流式细胞术测量稳定的肺移植患者(n=38)、BOS 患者(n=20)和健康对照者(n=10)的 T 细胞中的共刺激分子、颗粒酶 B、穿孔素和细胞内细胞因子。与稳定的患者相比,BOS 患者的 T 细胞中产生颗粒酶 B、干扰素(IFN)-γ 和肿瘤坏死因子(TNF)-α的 CD4/28(null)和 CD8/28(null)T 细胞的比例显著增加。CD28 的下调与类固醇耐药有关,CD4(+)T 细胞上的 CD134、CD137、CD152 和 CD154 以及 CD8(+)T 细胞上的 CD137 和 CD152 上调。增加的 CD28(null)/CD137 T 细胞产生 IFN-γ、TNF-α与 BOS 分级呈显著相关(r=0.861,P<0.001 用于 CD28(null)/CD137 IFN-γ/CD8)和移植后时间(r=0.698,P<0.001 用于 CD28(null)/CD137 IFN-γ/CD8)。BOS 与类固醇耐药的外周血前炎性 CD4(+)和 CD8(+)T 细胞上 CD28 的下调和替代共刺激分子的上调有关。外周血 CD28(null)T 细胞上替代共刺激分子的治疗性靶向以及使用这些检测方法监测反应可能有助于 BOS 患者的管理。