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Aging diminishes the resistance of AO rats to EAE: putative role of enhanced generation of GM-CSF Expressing CD4+T cells in aged rats
dc.creator | Stojić-Vukanić, Zorica | |
dc.creator | Nacka-Aleksić, Mirjana | |
dc.creator | Pilipović, Ivan | |
dc.creator | Vujnović, Ivana | |
dc.creator | Blagojević, Veljko | |
dc.creator | Kosec, Duško | |
dc.creator | Dimitrijević, Mirjana | |
dc.creator | Leposavić, Gordana | |
dc.date.accessioned | 2021-02-18T10:44:31Z | |
dc.date.available | 2021-02-18T10:44:31Z | |
dc.date.issued | 2015 | |
dc.identifier.issn | 1742-4933 | |
dc.identifier.uri | http://intor.torlakinstitut.com/handle/123456789/430 | |
dc.description.abstract | Background: Aging influences immune response and susceptibility to EAE in a strain specific manner. The study was designed to examine influence of aging on EAE induction in Albino Oxford (AO) rats. Results: Differently from 3-month-old (young) rats, which were resistant to EAE induction, the majority of aged (24-26-month-old) rats developed mild chronic form of EAE. On 16th day post-immunization, when in aged rats the neurological deficit reached plateau, more mononuclear cells, including CD4+ T lymphocytes was retrieved from spinal cord of aged than young rats. The frequencies of IL-17+ and GM-CSF+ cells within spinal cord infiltrating CD4+ lymphocytes were greater in aged rats. To their increased frequency contributed the expansion of GM-CSF + IL-17 + IFN-gamma+ cells, which are highly pathogenic in mice. The expression of the cytokines (IL-1 beta and IL-23/p19) driving GM-CSF + IL-17 + IFN-gamma + cell differentiation in mice was also augmented in aged rat spinal cord mononuclear cells. Additionally, in aged rat spinal cord the expansion of GM-CSF + IL-17-IFN-gamma- CD4+ T lymphocytes was found. Consistently, the expression of mRNAs for IL-3, the cytokine exhibiting the same expression pattern as GM-CSF, and IL-7, the cytokine driving differentiation of GM-CSF + IL-17-IFN-gamma- CD4 + lymphocytes in mice, was upregulated in aged rat spinal cord mononuclear cells, and the tissue, respectively. This was in accordance with the enhanced generation of the brain antigen-specific GM-CSF+ CD4+ lymphocytes in aged rat draining lymph nodes, as suggested by (i) the higher frequency of GM-CSF+ cells (reflecting the expansion of IL-17-IFN-gamma- cells) within their CD4+ lymphocytes and (ii) the upregulated GM-CSF and IL-3 mRNA expression in fresh CD4+ lymphocytes and MBP-stimulated draining lymph node cells and IL-7 mRNA in lymph node tissue from aged rats. In agreement with the upregulated GM-CSF expression in aged rats, strikingly more CD11b + CD45(int) (activated microglia) and CD45(hi) (mainly proinflammatory dendritic cells and macrophages) cells was retrieved from aged than young rat spinal cord. Besides, expression of mRNA for SOCS1, a negative regulator of proinflammatory cytokine expression in innate immunity cells, was downregulated in aged rat spinal cord mononuclear cells. Conclusions: The study revealed that aging may overcome genetic resistance to EAE, and indicated the cellular and molecular mechanisms contributing to this phenomenon in AO rats. | en |
dc.publisher | BMC, London | |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175050/RS// | |
dc.rights | openAccess | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.source | Immunity & Ageing | |
dc.subject | AO rats | en |
dc.subject | Aging | en |
dc.subject | EAE | en |
dc.subject | GM-CSF | en |
dc.title | Aging diminishes the resistance of AO rats to EAE: putative role of enhanced generation of GM-CSF Expressing CD4+T cells in aged rats | en |
dc.type | article | |
dc.rights.license | BY | |
dc.citation.other | 12 | |
dc.citation.rank | M22 | |
dc.citation.volume | 12 | |
dc.identifier.doi | 10.1186/s12979-015-0044-x | |
dc.identifier.fulltext | http://intor.torlakinstitut.com/bitstream/id/262/427.pdf | |
dc.identifier.pmid | 26448779 | |
dc.identifier.scopus | 2-s2.0-84943429482 | |
dc.identifier.wos | 000362407400001 | |
dc.type.version | publishedVersion |