Interferon-γ mRNA expression upon in vitro T lymphocyte activation is decreased in rheumatoid arthritis patients

Reduced interferon-gamma (IFN-γ) secretion with increased IFN-γ mRNA expression in atopic dermatitis: evidence for a post-transcriptional defect

“…As IFN-7 seeretion is considered to be primarily regulated by the rate of gene transcription [17][18][19], it was possible that expression of IFN-7 mRNA in atopic individuals would be reduced. A signifieant finding in this study was the presence of IFN-7 mRNA in [20][21][22][23][24][25], Similar findings have been confirmed using the more sensitive technique of PCR-assisted mRNA amplification which we employed in this study [13.14]. Our fmding that controls did not express IFN--) mRNA in freshly isolated PBMC or unstimulaled cultures is consistent with these previous reports.…”

“…In previous reports examining IFN-7 mRNA expression in PBMC or Tcell cultures from healthy adults and neonates by Northern analysis. transcripts have only been detected following stimulation in vitro [20][21][22][23][24][25], Similar findings have been confirmed using the more sensitive technique of PCR-assisted mRNA amplification which we employed in this study [13.14]. Our fmding that controls did not express IFN--) mRNA in freshly isolated PBMC or unstimulaled cultures is consistent with these previous reports.…”

Aberrant regulation of interleukin‐12 receptor β2 chain on type 1 cytokine‐stimulated T lymphocytes in type 1 diabetes

“…A regulatory defect characterized by a decreased IFN‐γ response has been suggested to be associated with T1D, 7 although the mechanisms of the defect have not been identified. In rheumatoid arthritis and spondyloarthropathy, a decreased IFN‐γ response is seen in peripheral blood and in synovial‐derived T cells, which is recovered after treatment with anti‐TNF‐α associated with clinical remission 20–22 . Accordingly, the possibility that a decreased type 1 response of peripheral blood T cells is associated with the regulatory defect leading to clinical manifestation of autoimmune diseases should be considered in future studies.…”

Cytokine and chemokine receptor profile of peripheral blood mononuclear cells during treatment with infliximab in patients with active rheumatoid arthritis

“…[16][17][18] The TNFa blockade normalised the mitogen response of PBMC as shown by the normal production of both IFNc and IL4. Activation of type 1 immune response, described as an increase in the number of PBMC spontaneously producing IFNc after 4 weeks of treatment with etanercept, a soluble TNF receptor, has been reported earlier by Berg et al 11 Also IFNc production of PBMC stimulated with microbial antigens (purified protein derivative, influenza virus) or autoantigen (collagen type II) increased in the patients during treatment.…”