Reduced IL-2 but elevated IL-4, IL-6, and IgE serum levels in patients with cerebral infarction during the acute stage

被引:84
作者
Kim, HM
Shin, HY
Jeong, HJ
An, HJ
Kim, NS
Chae, HJ
Kim, HR
Song, HJ
Kim, KY
Baek, SH
Cho, KH
Moon, BS
Lee, YM [1 ]
机构
[1] Wonkwang Univ, Coll Pharm, Oriental Med Res Ctr, Dept Oriental Pharm, Iksan 570749, Chonbuk, South Korea
[2] Wonkwang Univ, Sch Med, Iksan 570749, Chonbuk, South Korea
[3] Wonkwang Univ, Sch Dent, Dept Dent Pharmacol, Iksan 570749, Chonbuk, South Korea
[4] Wonkwang Univ, Coll Oriental Med, Iksan 570749, Chonbuk, South Korea
[5] Wonkwang Univ, Profess Grad Sch Oriental Med, Iksan 570749, Chonbuk, South Korea
关键词
IFN-gamma; IL-2; IL-4; IL-6; IgE; cerebral infarction;
D O I
10.1385/JMN:14:3:191
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cytokines in the central nervous system (CNS) may play an important role in functioning as intercellular signals that orchestrate the response to injury. Whether this is a cause or result of the brain disease process is uncertain. We investigated IFN-gamma, IL-2, IL-4, IL-6, and IgE in the sera of 38 patients with cerebral infarction during the acute stage and 10 normal controls using an originally devised sensitive sandwich enzyme-linked immunosorbent assay (ELISA). We found that serum levels of IL-2 derived from T helper 1 (Th1) cells were slightly reduced in patients with cerebral infarction, whereas serum levels of IL-4 and IL-6 derived from Th2 cells were elevated significantly. IL-4 induces synthesis of IgE in human B cells. Endogenous IL-6 plays an obligatory role in IL-4-dependent human IgE synthesis. We observed that serum IgE levels were elevated significantly in patients with cerebral infarction. However, serum IFN-gamma levels were not elevated significantly in cerebral infarction patients. These findings suggest that elevated IL-4, IL-6, and IgE levels in the human serum may be an important factor in cerebral infarction during the acute stage. Decrease of IL-2 levels in the serum of patients with cerebral infarction may be a regulatory mechanism.
引用
收藏
页码:191 / 196
页数:6
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