T cell chemokine receptor expression in human Th1- and Th2-associated diseases.
T cell chemokine receptor expression in human Th1- and Th2-associated diseases.
复制标题
人类 Th1 和 Th2 相关疾病中 T 细胞趋化因子受体的表达。
DOI:
10.1007/978-94-015-9702-9_3
复制
发表时间:
2000
影响因子:
3.2
通讯作者:
K. HayGlass
中科院分区:
文献类型:
--
作者:
J. D. Campbell;K. HayGlass
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2-associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3, while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1- and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
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DOI:
10.1164/ajrccm.160.6.9811089
发表时间:
1999-12-01
影响因子:
24.7
作者:
Nakamura, H;Weiss, ST;Lilly, CM
通讯作者:
Lilly, CM
影响因子:
158.5
作者:
Trapp, BD;Peterson, J;Bö, L
通讯作者:
Bö, L
影响因子:
4.4
作者:
W. Karpus;N. Lukacs;K. J. Kennedy;W. S. Smith;S. Hurst;T. Barrett
通讯作者:
W. Karpus;N. Lukacs;K. J. Kennedy;W. S. Smith;S. Hurst;T. Barrett
DOI:
10.1073/pnas.96.12.6873
发表时间:
1999-06-08
影响因子:
11.1
作者:
Balashov, KE;Rottman, JB;Hancock, WW
通讯作者:
Hancock, WW