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超敏性肺炎中肺脏CD8 + CD56 +自然杀伤T细胞的扩增

Expansion of pulmonary CD8+CD56+ natural killer T-cells in hypersensitivity pneumonitis.

作者信息

Korosec Peter, Osolnik Katarina, Kern Izidor, Silar Mira, Mohorcic Katja, Kosnik Mitja

机构信息

Laboratory of Immunology and Molecular Biology, University Clinic of Respiratory and Allergic Diseases, Golnik, Slovenia.

出版信息

Chest. 2007 Oct;132(4):1291-7. doi: 10.1378/chest.07-0128. Epub 2007 Jul 23.

Abstract

BACKGROUND

Natural killer T (NKT) cells, a newly identified subgroup of T cells with immunoregulatory function, may be implicated in the pathogenesis of interstitial lung disease (ILD).

METHODS

We used multiparameter flow cytometry with antibodies to CD3, CD4, CD8, CD14, CD19, CD45, CD16/56, CD56, CD161, and Valpha24 invariant T-cell receptor (TCR) in BAL fluid (BALF) to examine the frequency and distribution of pulmonary NKT cells in several cases of ILD. We included 57 patients with sarcoidosis and 17 patients with hypersensitivity pneumonitis.

RESULTS

We found significantly higher frequencies of pulmonary NKT cells in patients with hypersensitivity pneumonitis in comparison to the other study patients with ILD (median proportion of NKT cells, 11%; range, 3 to 38%; vs 3%; range, 0 to 16%; p < 0.0001). In contrast, there was no difference in the proportion of conventional natural killer cells. We found that a major subset of NKT cells in the BALF of patients with hypersensitivity pneumonitis was a CD8+CD56+ population that did not express the invariant TCR.

CONCLUSIONS

These results suggest the involvement of NKT cells in the pathogenesis of hypersensitivity pneumonitis.

摘要

背景

自然杀伤T(NKT)细胞是新发现的具有免疫调节功能的T细胞亚群,可能与间质性肺病(ILD)的发病机制有关。

方法

我们使用多参数流式细胞术,采用针对支气管肺泡灌洗液(BALF)中CD3、CD4、CD8、CD14、CD19、CD45、CD16/56、CD56、CD161和Vα24恒定T细胞受体(TCR)的抗体,检测数例ILD患者肺内NKT细胞的频率和分布。我们纳入了57例结节病患者和17例过敏性肺炎患者。

结果

我们发现,与其他ILD研究患者相比,过敏性肺炎患者肺内NKT细胞频率显著更高(NKT细胞的中位比例为11%;范围为3%至38%;相比之下为3%;范围为0%至16%;p<0.0001)。相比之下,常规自然杀伤细胞的比例没有差异。我们发现,过敏性肺炎患者BALF中NKT细胞的一个主要亚群是不表达恒定TCR的CD8+CD56+群体。

结论

这些结果提示NKT细胞参与了过敏性肺炎的发病机制。

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