Estrogen augments the T cell-dependent but not the T-independent immune response

被引:38
作者
Adori, Monika [1 ]
Kiss, Endre [4 ]
Barad, Zsuzsanna [1 ,2 ]
Barabas, Klaudia [3 ]
Kiszely, Edda [1 ]
Schneider, Andrea [1 ]
Sziksz, Erna [1 ]
Abraham, Istvan M. [2 ]
Matko, Janos [1 ,4 ]
Sarmay, Gabriella [1 ,4 ]
机构
[1] Eotvos Lorand Univ, Dept Immunol, Budapest, Hungary
[2] Univ Otago, Dept Physiol, Ctr Neuroendocrinol, Dunedin, New Zealand
[3] Eotvos Lorand Univ, Inst Biol, Prote Lab, Budapest, Hungary
[4] Eotvos Lorand Univ, Hungarian Acad Sci, Immunol Res Grp, Budapest, Hungary
关键词
B cells; Antibody production; TD and TI-2 antigen; Estrogen receptors; Cell activation; Signal transduction; NF-KAPPA-B; AUTOIMMUNE-DISEASE; RECEPTOR-ALPHA; INTRACELLULAR CALCIUM; TRAUMA-HEMORRHAGE; PLASMA-MEMBRANE; SEX-DIFFERENCES; IN-VIVO; ACTIVATION; ESTRADIOL;
D O I
10.1007/s00018-010-0270-5
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
Estrogen plays a critical regulatory role in the development and maintenance of immunity. Its role in the regulation of antibody synthesis in vivo is still not completely clear. Here, we have compared the effect of estrogen on T cell-dependent (TD) and T cell-independent type 2 (TI-2) antibody responses. The results provide the first evidence that estrogen enhances the TD but not the TI-2 response. Ovariectomy significantly decreased, while estrogen re-administration increased the number of hapten-specific IgM- and IgG-producing cells in response to TD antigen. In vitro experiments also show that estrogen may have a direct impact on B and T cells by inducing rapid signaling events, such as Erk and AKT phosphorylation, cell-specific Ca(2+) signal, and NF kappa B activation. These non-transcriptional effects are mediated by classical estrogen receptors and partly by an as yet unidentified plasma membrane estrogen receptor. Such receptor- mediated rapid signals may modulate the in vivo T cell-dependent immune response.
引用
收藏
页码:1661 / 1674
页数:14
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