V alpha 24-invariant NKT cells from patients with allergic asthma express CCR9 at high frequency and induce Th2 bias of CD3(+) T cells upon CD226 engagement

	V alpha 24-invariant NKT cells from patients with allergic asthma express CCR9 at high frequency and induce Th2 bias of CD3(+) T cells upon CD226 engagement
	Yang, S; Bi, YY; He, YL; Xie, LK; He, L; Xiong, J; Deng, T; Zhou, G; Liu, JY; Hu, CS
刊名	JOURNAL OF IMMUNOLOGY
	2005
卷号	175 期号:8 页码:4914-4926
通讯作者	Tan, JQ (reprint author), Anhui Med Univ, Dept Immunol, Hefei, Peoples R China.,immu_jin@fmmu.edu.cn ; jinquan_tan@hotmail.com
英文摘要	We have demonstrated that V alpha 24(+)V beta 11(+) invariant (V alpha 24(+)i) NKT cells from patients with allergic asthma express CCR9 at high frequency. CCR9 ligand CCL25 induces chemotaxis of asthmatic Va24+i NKT cells but not the normal cells. A large number of CCR9-positive V alpha 24(+)i NKT cells are found in asthmatic bronchi mucosa, where high levels of Th2 cytokines are detected. Asthmatic V alpha 24(+)i NKT cells, themselves Th1 biased, induce CD3(+) T cells into an expression of Th2 cytokines (IL-4 and IL-13) in cell-cell contact manner in vitro. CD226 are overexpressed on asthmatic V alpha 24(+)i NKT cells. CCL25/CCR9 ligation causes directly phosphorylation of CD226, indicating that CCL25/CCR9 signals can cross-talk with CD226 signals to activate V alpha 24(+)i NKT cells. Prestimulation with immobilized CD226 mAb does not change ability of asthmatic V alpha 24(+)i NKT cells to induce Th2-cytokine production, whereas soluble CD226 mAb or short hairpin RNA of CD226 inhibits V alpha 24(+)i NKT cells to induce Th2-cytokine production by CD3(+) T cells, indicating that CD226 engagement is necessary for V alpha 24(+)i NKT cells to induce Th2 bias of CD3(+) T cells. Our results are providing with direct evidence that aberration of CCR9 expression on asthmatic V alpha 24(+)i NKT cells. CCL25 is first time shown promoting the recruitment of CCR9-expressing V alpha 24(+)i NKT cells into the lung to promote other T cells to produce Th2 cytokines to establish and develop allergic asthma. Our findings provide evidence that abnormal asthmatic V alpha 24(+)i NKT cells induce systemically and locally a Th2 bias in T cells that is at least partially critical for the pathogenesis of allergic asthma.
学科主题	Immunology
类目[WOS]	Immunology
关键词[WOS]	CHEMOKINE RECEPTOR EXPRESSION ; PERIPHERAL-BLOOD LYMPHOCYTES ; HUMAN DENDRITIC CELLS ; REGULATORY PROPERTIES ; ADHESION MOLECULE ; DISTINCT SUBSETS ; CYTOKINE PROFILE ; CUTTING EDGE ; ALPHA ; DNAM-1
收录类别	SCI
语种	英语
WOS记录号	WOS:000232443500012
内容类型	期刊论文
版本	出版稿
源URL	[http://202.127.25.143/handle/331003/1942]
专题	上海生化细胞研究所_上海生科院生化细胞研究所
推荐引用方式 GB/T 7714	Yang, S,Bi, YY,He, YL,et al. V alpha 24-invariant NKT cells from patients with allergic asthma express CCR9 at high frequency and induce Th2 bias of CD3(+) T cells upon CD226 engagement[J]. JOURNAL OF IMMUNOLOGY,2005,175(8):4914-4926.
APA	Yang, S.,Bi, YY.,He, YL.,Xie, LK.,He, L.,...&Tan, JQ.(2005).V alpha 24-invariant NKT cells from patients with allergic asthma express CCR9 at high frequency and induce Th2 bias of CD3(+) T cells upon CD226 engagement.JOURNAL OF IMMUNOLOGY,175(8),4914-4926.
MLA	Yang, S,et al."V alpha 24-invariant NKT cells from patients with allergic asthma express CCR9 at high frequency and induce Th2 bias of CD3(+) T cells upon CD226 engagement".JOURNAL OF IMMUNOLOGY 175.8(2005):4914-4926.