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http://purl.uniprot.org/citations/22248722http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22248722http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

Stress-induced rise in circulating catecholamines (CAs), followed by modulation of β-adrenergic receptors (adrenoceptors, ARs), is one of the pathways involved in the stress-mediated effects of immune functions. The spleen is an organ with a high number of lymphocytes and provides a unique microenvironment in which they reside. Thus, lymphocytes may respond differently to CAs in the spleen than in the circulation. No reports exist concerning the involvement of β-ARs in stress-mediated effects on T and B cells isolated from the spleen. Therefore, our aim was to investigate the effect of single stress exposure on gene expression and cellular localization of β-adrenoceptor subtypes in splenic T and B cells. We tried to correlate changes in adrenoceptors with the expression of apoptotic proteins.

Methods

Immobilization (IMMO) was used as a stress model. T and B cells were isolated from rat spleen using magnetically labeled antibodies. The gene expression of individual adrenoceptors and apoptotic proteins was evaluated by real-time PCR. Immunofluorescence was used to evaluate localization and adrenoceptor expression.

Results

We have found T cells to be more vulnerable to stress compared to B cells, because of increased β₁-, β₂- and β₃-ARs after a single IMMO. Moreover, β₂-ARs translocated from the nucleus to the plasma membrane in T cells after IMMO. The rise in β-ARs most probably led to the rise of Bax mRNA and Bax to Bcl-2 mRNA ratio. This might suggest the induction of an apoptotic process in T cells.

Conclusion

Higher susceptibility of T cells to stress via modulation of β-ARs and apoptotic proteins might shift the immune responsiveness in the spleen."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.org/dc/terms/identifier"doi:10.1159/000329002"xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Krizanova O."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Vargovic P."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Kvetnansky R."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Imrich R."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Laukova M."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Csaderova L."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Chovanova L."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/author"Vlcek M."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/name"Neuroimmunomodulation"xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/pages"69-78"xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/title"Acute stress differently modulates beta1, beta2 and beta3 adrenoceptors in T cells, but not in B cells, from the rat spleen."xsd:string
http://purl.uniprot.org/citations/22248722http://purl.uniprot.org/core/volume"19"xsd:string
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