Tsurikisawa Naomi, Saito Hiroshi, Tsuburai Takahiro, Oshikata Chiyako, Ono Emiko, Mitomi Hiroyuki, Akiyama Kazuo
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization Sagamihara National Hospital, Kanagawa, Japan.
J Allergy Clin Immunol. 2008 Sep;122(3):610-6. doi: 10.1016/j.jaci.2008.05.040. Epub 2008 Jun 30.
Chronic eosinophilic pneumonia (CEP) with asthma precedes the onset of Churg-Strauss syndrome (CSS) in half of all patients with CSS. It is not known what determines whether patients with CEP after asthma will have CSS.
We examined whether activation of regulatory T cells in patients with CEP inhibits CSS development and is otherwise involved in the mechanism of CSS disease.
In patients with CSS (n = 38), CEP with asthma (n = 20), and general adult asthma (n = 108), we examined the number of CD4(+)CD25(+) T cells in peripheral blood, as well as levels of expression of the cytokines IL-2, IL-5, IL-10, and TGF-beta by CD4(+)CD25(+) T cells, CD4(+)CD25(-) T cells, or both.
At disease onset, patients with CSS, unlike patients with CEP, had significantly fewer CD4(+)CD25(+) T cells than patients with any step of asthma. CD4(+)CD25(+) T cells producing IL-10 were rarely detected in patients with CSS at disease onset or relapse, whereas the numbers of IL-10-producing T cells in patients with CEP were high at disease onset. There were fewer CD4(+)CD25(-) T cells producing IL-2 in patients with CSS before treatment than in patients with CEP at disease onset. The proportions of CD4(+)CD25(+) T cells producing IL-10 and CD4(+)CD25(-) T cells producing IL-2 in patients with CSS increased at remission.
Maintenance of the numbers of regulatory T cells in patients with CEP with asthma might inhibit CSS development through the action of cytokines, such as IL-10 and IL-2, produced by CD4(+)CD25(+) or CD4(+)CD25(-) T cells. This might be part of a mechanism that influences progression and prognosis in these diseases.
在所有变应性肉芽肿性血管炎(CSS)患者中,半数患者在哮喘之后会出现慢性嗜酸性粒细胞性肺炎(CEP)。目前尚不清楚是什么决定了哮喘后发生CEP的患者是否会发展为CSS。
我们研究了CEP患者中调节性T细胞的激活是否会抑制CSS的发展,以及是否参与了CSS疾病的发病机制。
我们检测了CSS患者(n = 38)、合并哮喘的CEP患者(n = 20)和普通成年哮喘患者(n = 108)外周血中CD4(+)CD25(+) T细胞的数量,以及CD4(+)CD25(+) T细胞、CD4(+)CD25(-) T细胞或两者产生的细胞因子IL-2、IL-5、IL-10和TGF-β的表达水平。
在疾病发作时,与CEP患者不同,CSS患者的CD4(+)CD25(+) T细胞数量明显少于任何阶段的哮喘患者。在疾病发作或复发时,CSS患者中很少检测到产生IL-10的CD4(+)CD25(+) T细胞,而CEP患者在疾病发作时产生IL-10的T细胞数量较高。治疗前,CSS患者中产生IL-2的CD4(+)CD25(-) T细胞数量少于疾病发作时的CEP患者。CSS患者缓解期产生IL-10的CD4(+)CD25(+) T细胞和产生IL-2的CD4(+)CD25(-) T细胞比例增加。
合并哮喘的CEP患者中调节性T细胞数量的维持可能通过CD4(+)CD25(+)或CD4(+)CD25(-) T细胞产生的细胞因子(如IL-10和IL-2)的作用来抑制CSS的发展。这可能是影响这些疾病进展和预后的机制的一部分。