Estrogen augments the T cell-dependent but not the T-independent immune response
| Autor: | Andrea E. Schneider, Erna Sziksz, Klaudia Barabás, János Matkó, István M. Ábrahám, Endre Kiss, Zsuzsanna Barad, Edda Kiszely, Mónika Ádori, Gabriella Sármay |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
Membrane estrogen receptor Transcription Genetic medicine.drug_class T cell Ovariectomy T-Lymphocytes Estrogen receptor Biology Cellular and Molecular Neuroscience Interferon-gamma Mice Immune system Antigen Internal medicine medicine Animals Calcium Signaling Phosphorylation Receptor Extracellular Signal-Regulated MAP Kinases Molecular Biology Estrogen receptor beta Pharmacology Cell Nucleus B-Lymphocytes Estradiol Immunity NF-kappa B Cell Biology Cell biology Enzyme Activation Mice Inbred C57BL Protein Transport Endocrinology medicine.anatomical_structure Receptors Estrogen Estrogen Antibody Formation Molecular Medicine Female Proto-Oncogene Proteins c-akt |
| Zdroj: | Cellular and molecular life sciences : CMLS. 67(10) |
| ISSN: | 1420-9071 |
| Popis: | 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 NFkappaB 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. |
| Databáze: | OpenAIRE |
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