Browsing by Author "Mostarica-Stojković, M. (6701741422)"
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Publication Rat NKR-P1 + CD3 + T cells: Selective proliferation in interleukin-2, diverse T-cell-receptor-Vβ repertoire and polarized interferon-γ expression(1998) ;Badovinac, V. (6603057711) ;Boggiano, C. (6701588802) ;Trajković, V. (7004516866) ;Frey, A.B. (7102846668) ;Vujanović, N.L. (7003467079) ;Gold, D.P. (7201806702) ;Mostarica-Stojković, M. (6701741422)Vukmanović, S. (35552076100)Cells expressing markers of both natural killer and T lymphocytes (NK T cells) in humans and mice express a restricted T-cell receptor (TCR) repertoire, are of CD4 - CD8 - or CD4 + CD 8- phenotype, and upon anti-CD3 stimulation secrete large amounts of interleukin-4 (IL-4) and interferon-γ (IFN-γ). NK T cells may be the primary source of IL-4-promoting T helper type 2 (Th2) responses and/or they might be involved in regulating the balance between Th1- and Th2-type immune responses, and may consequently affect susceptibility to autoimmune diseases associated with a skewed Th phenotype. We show that rat NK T cells selectively proliferate to IL-2, and sse this fact to analyse cytokine production by NK T cells in two rat strains differentially susceptible to Th1- or Th2-type autoimmune diseases. Analysis by reverse transcription-polymerase chain reaction revealed that, in contrast to mouse, rat NK T cells secrete exclusively IFN-γ and not IL-4 after anti- CD3 stimulation, and use a wider TCR-Vβ repertoire, suggesting that rat NK T cells are not essential for the development of Th2-type CD4 + T-cell responses. - Some of the metrics are blocked by yourconsent settings
Publication Rat NKR-P1 + CD3 + T cells: Selective proliferation in interleukin-2, diverse T-cell-receptor-Vβ repertoire and polarized interferon-γ expression(1998) ;Badovinac, V. (6603057711) ;Boggiano, C. (6701588802) ;Trajković, V. (7004516866) ;Frey, A.B. (7102846668) ;Vujanović, N.L. (7003467079) ;Gold, D.P. (7201806702) ;Mostarica-Stojković, M. (6701741422)Vukmanović, S. (35552076100)Cells expressing markers of both natural killer and T lymphocytes (NK T cells) in humans and mice express a restricted T-cell receptor (TCR) repertoire, are of CD4 - CD8 - or CD4 + CD 8- phenotype, and upon anti-CD3 stimulation secrete large amounts of interleukin-4 (IL-4) and interferon-γ (IFN-γ). NK T cells may be the primary source of IL-4-promoting T helper type 2 (Th2) responses and/or they might be involved in regulating the balance between Th1- and Th2-type immune responses, and may consequently affect susceptibility to autoimmune diseases associated with a skewed Th phenotype. We show that rat NK T cells selectively proliferate to IL-2, and sse this fact to analyse cytokine production by NK T cells in two rat strains differentially susceptible to Th1- or Th2-type autoimmune diseases. Analysis by reverse transcription-polymerase chain reaction revealed that, in contrast to mouse, rat NK T cells secrete exclusively IFN-γ and not IL-4 after anti- CD3 stimulation, and use a wider TCR-Vβ repertoire, suggesting that rat NK T cells are not essential for the development of Th2-type CD4 + T-cell responses. - Some of the metrics are blocked by yourconsent settings
Publication The role of T-lymphocyte subsets in susceptibility and resistance to induction of autoimmunity in the central nervous system; [Uloga subpopulacija T limfocita u osetljivosti i otpornosti na indukciju autoimunosti u centralnom nervnom sistemu.](1994) ;Mostarica-Stojković, M. (6701741422) ;Vukmanović, S. (35552076100) ;Radojković, M. (57200867308) ;Ramić, Z. (6603943950) ;Vucković, S. (7003869325) ;Ejdus, L. (6603639561) ;Pravica, V. (7003322504) ;Simić, M.M. (7005712358)Lukić, M.L. (7005792112)The importance of two major subsets of T cells (CD4 and CD8) for the induction of EAE was analysed in two strains of rats differing in susceptibility to EAE and the level of IL 2 production. It was found that CD8 cells do not play a role in the induction or in the inherent resistance to EAE. Additionally, the elimination of CD8 cells does not increase the IL 2 production in lymphoid cell cultures. Based on these and previous results showing that a low dose of cyclophosphamide readily abrogates the resistance to EAE and enhances the IL 2 production. Thus it was concluded that genetically determined differences in susceptibility to EAE are governed by immunoregulatory genes whose effect appears to be mediated at the level of cellular interaction of different subsets of CD4 T cells.
