Estrogen Regulates CCR Gene Expression and Function in T Lymphocytes

Estrogen has been implicated in the observed female bias in autoimmune diseases. However, the mechanisms behind this gender dimorphism are poorly defined. We have previously reported that in vivo T cell trafficking is gender- and estrogen-dependent. Chemokine receptors are critical determinants of T...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2005-05, Vol.174 (10), p.6023-6029
Main Authors: Mo, RuRan, Chen, Jun, Grolleau-Julius, Annabelle, Murphy, Hedwig S, Richardson, Bruce C, Yung, Raymond L
Format: Article
Language:English
Subjects:
Animals
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - metabolism
Cell Line
Chemokine CCL3
Chemokine CCL4
Chemokine CXCL12
Chemokines, CC - metabolism
Chemokines, CXC - pharmacology
Chemotaxis, Leukocyte - immunology
Estrogens - administration & dosage
Estrogens - physiology
Female
Gene Expression Regulation - immunology
Macrophage Inflammatory Proteins - pharmacology
Male
Mice
Mice, Inbred AKR
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred DBA
Ovariectomy
Receptors, CCR4
Receptors, CCR5 - biosynthesis
Receptors, CCR5 - genetics
Receptors, CCR5 - physiology
Receptors, Chemokine - biosynthesis
Receptors, Chemokine - genetics
Receptors, Chemokine - physiology
Sex Characteristics
Species Specificity
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
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Summary:Estrogen has been implicated in the observed female bias in autoimmune diseases. However, the mechanisms behind this gender dimorphism are poorly defined. We have previously reported that in vivo T cell trafficking is gender- and estrogen-dependent. Chemokine receptors are critical determinants of T cell homing and immune response. In this study, we show that the female gender is associated with increased CD4(+) T cell CCR1-CCR5 gene and protein expression in mice. The increased CCR expression correlates with enhanced in vitro chemotaxis response to MIP-1beta (CCL4). In vivo treatment of young oophorectomized and postmenopausal female mice with 17beta-estradiol also increased CD4(+) T cell CCR expression. Finally, 17beta-estradiol enhances tyrosine phosphorylation in T cells stimulated with MIP-1alpha in a time-dependent manner. Our results indicate an important role of estrogen in determining T cell chemokine response that may help explain the increased susceptibility and severity of autoimmune diseases in females.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.174.10.6023