Estrogen and CD4+ T cells

被引:101
作者
Pernis, Alessandra B. [1 ]
机构
[1] Columbia Univ, Dept Med, New York, NY 10032 USA
关键词
estrogen; systemic lupus erythematosus; T cell;
D O I
10.1097/BOR.0b013e328277ef2a
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Many autoimmune rheumatic autoimmune disorders predominantly affect women. Sex hormones, in particular estrogen, can influence CD4(+) T-helper development and function. We highlight recent studies that begin to provide insights into the mechanisms by which estrogen modulates CD4(+) T-cell development and function, and thus potentially contribute to disease pathogenesis. Recent findings High levels of estrogen can lead to thymic atrophy. Recent studies showed that this phenomenon results from effects of estrogen at multiple stages in early T-cell development. Estrogen is also known to affect mature CD4(+) T-cell function, and, in particular, their ability to produce selected cytokine profiles. The mechanisms by which estrogen can exert these effects were also recently explored and shown to include effects on expression of critical molecules known to be involved in these processes. Summary Dissecting the molecular pathways employed by estrogen to modulate CD4(+) T cells will be critical in elucidating the manner by which estrogen exerts its effects on this compartment. Given that cell type specific differences underlie the ability of many hormonal therapies to exert tissue-specific estrogenic or antiestrogenic activities, this knowledge will be crucial to further exploitation of hormonal therapies in rheumatic autoimmune diseases.
引用
收藏
页码:414 / 420
页数:7
相关论文
共 98 条
[1]   Estrogen and tamoxifen induce cytoskeletal remodeling and migration in endometrial cancer cells [J].
Acconcia, F ;
Barnes, CJ ;
Kumar, R .
ENDOCRINOLOGY, 2006, 147 (03) :1203-1212
[2]   Late onset of treatment with a chemokine receptor CCR1 antagonist prevents progression of lupus nephritis in MRL-Fas(lpr) mice [J].
Anders, HJ ;
Belemezova, E ;
Eis, V ;
Segerer, S ;
Vielhauer, V ;
De Lema, GP ;
Kretzler, M ;
Cohen, CD ;
Frink, M ;
Horuk, R ;
Hudkins, KL ;
Alpers, CE ;
Mampaso, F ;
Schlöndorff, D .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2004, 15 (06) :1504-1513
[3]   Molecular mechanisms for gender differences in susceptibility to T cell-mediated autoimmune diabetes in nonobese diabetic mice [J].
Bao, M ;
Yang, Y ;
Jun, HS ;
Yoon, JW .
JOURNAL OF IMMUNOLOGY, 2002, 168 (10) :5369-5375
[4]   Low-dose estrogen therapy ameliorates experimental autoimmune encephalomyelitis in two different inbred mouse strains [J].
Bebo, BF ;
Fyfe-Johnson, A ;
Adlard, K ;
Beam, AG ;
Vandenbark, AA ;
Offner, H .
JOURNAL OF IMMUNOLOGY, 2001, 166 (03) :2080-2089
[5]   Estradiol binding to cell surface raises cytosolic free calcium in T cells [J].
Benten, WPM ;
Lieberherr, M ;
Giese, G ;
Wunderlich, F .
FEBS LETTERS, 1998, 422 (03) :349-353
[6]   A FUNCTIONAL DICHOTOMY IN CD4+ LYMPHOCYTES-T [J].
BOTTOMLY, K .
IMMUNOLOGY TODAY, 1988, 9 (09) :268-274
[7]   Tissue distribution of estrogen receptors alpha (ER-alpha) and beta (ER-beta) mRNA in the midgestational human fetus [J].
Brandenberger, AW ;
Tee, MK ;
Lee, JY ;
Chao, V ;
Jaffe, RB .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1997, 82 (10) :3509-3512
[8]   The effects of pregnancy on autoimmune diseases [J].
Buyon, JP .
JOURNAL OF LEUKOCYTE BIOLOGY, 1998, 63 (03) :281-287
[9]  
Correale J, 1998, J IMMUNOL, V161, P3365
[10]   Early growth response-1 is required for CD154 transcription [J].
Cron, RQ ;
Bandyopadhyay, R ;
Genin, A ;
Brunner, M ;
Kersh, GJ ;
Yin, JY ;
Finkel, TH ;
Crow, MK .
JOURNAL OF IMMUNOLOGY, 2006, 176 (02) :811-818