Th17 immune responses contribute to the pathophysiology of aplastic anemia

被引：151

作者：

de Latour, Regis Peffault ^{[1
,2
]}

Visconte, Valeria

Takaku, Tomoiku

Wu, Colin ^{[3
]}

Erie, Andrew J.

Sarcon, Annahita K.

Desierto, Marie J.

Scheinberg, Phillip

Keyvanfar, Keyvan

Nunez, Olga

Chen, Jichun

Young, Neal S.

机构：

[1] NHLBI, Hematol Branch, NIH, Clin Res Ctr, Bethesda, MD 20892 USA

[2] Greffe Hop St Louis, Serv Hematol, Paris, France

[3] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA

来源：

BLOOD | 2010年 / 116卷 / 20期

基金：

美国国家卫生研究院;

关键词：

BONE-MARROW FAILURE; REGULATORY T-CELLS; GROWTH-FACTOR-BETA; CLINICAL-RELEVANCE; FAMILY-MEMBERS; MOUSE MODEL; IL-17; DISEASE; INTERLEUKIN-17; INFLAMMATION;

D O I：

10.1182/blood-2010-01-266098

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

T helper type 17 (Th17) cells have been characterized based on production of interleukin-17 (IL-17) and association with autoimmune diseases. We studied the role of Th17 cells in aplastic anemia (AA) by isolating Th17 cells from patients blood (n = 41) and bone marrow (BM) mononuclear cells (n = 7). The frequency and total number of CD3(+)CD4(+)IL-17-producing T cells were increased in AA patients at presentation compared with healthy controls (P = .0007 and .02, respectively) and correlated with disease activity. There was an inverse relationship between the numbers of Th17 cells and CD4(+)CD25(high)FoxP3(+) regulatory T cells (Tregs) in the blood of AA patients. Concomitant with the classical Th1 response, we detected the presence of CD4(+) and CD8(+) IL-17-producing T cells in a mouse model of lymph node infusion-induced BM failure. Although anti-IL-17 treatment did not abrogate BM failure, early treatment with the anti-IL-17 antibody reduced the severity of BM failure with significantly higher platelet (P < .01) and total BM cell (P < .05) counts at day 10. Recipients that received anti-IL-17 treatment had significantly fewer Th1 cells (P < .01) and more Treg cells (P < .05) at day 10 after lymph node infusion. Th17 immune responses contribute to AA pathophysiology, especially at the early stage during disease progression. (Blood.2010;116(20):4175-4184)

引用

页码：4175 / 4184

页数：10

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