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  • 1
    Electronic Resource
    Electronic Resource
    Lipopolysaccharide Effectively Up-Regulates B7-1 (CD80) Expression and Costimulatory Function of Human Monocytes (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 42 (1995), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The influence of lipopolysaccharide (LPS) and various cytokines on the expression of the costimulatory molecule B7-1 and intercellular adhesion molecule-1 (ICAM-1), lymphocyte function associated antigen-3 (LFA-3) and human histocompatibility leucocyte antigen-DR (HLA-DR) on human monocytes and their effect on the costimulatory function was investigated. Freshly isolated human monocytes constitutively express ICAM-1, LFA-3 and HLA-DR, but no B7-1. B7-1 expression was up-regulated by LPS and, to a lesser extent, by interferon-γ (IFN-γ). The other stimuli tested, including IFN-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-α (TNF-α) and GM-CSF + TNF-α, did not influence expression of B7-1 on monocytes. ICAM-1 and HLA-DR were up-regulated by IFN-γ and LPS; LFA-3 expression was not influenced. LPS also effectively enhanced costimulatory function of monocytes as determined in the tetanustoxoid (TT) assay. Blocking of B7 by CTLA-4Ig inhibited the LPS-induced enhancement of costimulatory function almost completely. Our results indicate that the LPS-mediated up-regulation of the costimulatory function of human monocytes is mediated by B7. This mechanism may be important for host defence against Gram-negative bacteria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1995.tb03714.x
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  • 2
    Electronic Resource
    Electronic Resource
    Relationship between soluble tumor necrosis factor (TNF) receptors and TNFα during immunotherapy with interleukin-2 and/or interferon α (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 113-118 
    Details
    ISSN: 1432-0851
    Keywords: Soluble TNF receptors ; TNFα ; Immunotherapy ; IL-2 ; IFNα
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Eleven metastatic cancer patients were studied during three different regimens of immunotherapy with interleukin-2 (IL-2) and/or interferon α (IFNα): group A received 4 days of IL-2 i.a. infusion (n=3), group B IFNα s.c. during 5 days (n=4), followed on day 3 by 5 days of a continuous IL-2 i.v. infusion, and group C had 4 days of IL-2 i.v. infusion together with s.c. IFNα on days 1 and 4 (n=4). Soluble tumor necrosis factor receptors (sTNFR) p55 and p75 and TNFα concentrations in serum were analyzed before therapy and daily during 8 days of the first therapy cycle. sTNFR was measured by radioimmunoassay. sTNFR p55 increased in all patient groups from a baseline value of 5.2±0.9 ng/ml to a maximum of 13.6±1.2 ng/ml by days 3–4 (P=0.003). sTNFR p75 increased from 7.6±1.1 ng/ml to peak values of 30.1±2.6 ng/ml in groups A and B (P=0.02). In group C the sTNFR p75 response was weak (NS). In group B, the increase of both p55 and p75 occurred only after addition of IL-2 to IFNα. TNFα increased weakly during treatment with IFNα alone (group B); it rose strongly during IL-2 and the combined treatment (groups A-C) from 8±2 pg/ml to 115±13 pg/ml (P=0.003). In group B, it reached the maximum 24 h after addition of IL-2 to IFNα and decreased thereafter. there was a significant relationship between TNFα and sTNFR p55 or sTNFR p75 in groups A and C, (P=0.001), but not in group B. Group C was also investigated during the third therapy cycle. The increase of sTNFR p75 was stronger (P=0.01) and that of TNFα weaker than in the first cycle; the sTNFR p55 response was similar in both cycles. In conclusion sTNFR p55 and p75 are rapidly induced during IL-2 and IL-2+IFNα treatment, the increase of sTNF receptors parallels or exceeds that of TNFα and may influence the immunomodulatory effects of TNFα during cytokine therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01526206
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  • 3
    Electronic Resource
    Electronic Resource
    Relationship between soluble tumor necrosisfactor (TNF) receptors and TNFα during immunotherapywith interleukin-2 and/or interferon α (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 113-118 
    Details
    ISSN: 1432-0851
    Keywords: Key words: Soluble TNF receptors – TNFα– Immunotherapy – IL-2 – IFNα
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Eleven metastatic cancer patients were studied during three different regimens of immunotherapy with interleukin-2 (IL-2) and/or interferon α (IFNα): group A received 4 days of IL-2 i. a. infusion (n = 3), group B IFNα s.c. during 5 days (n = 4), followed on day 3 by 5 days of a continuous IL-2 i. v. infusion, and group C had 4 days of IL-2 i. v. infusion together with s. c. IFNα on days 1 and 4 (n = 4). Soluble tumor necrosis factor receptors (sTNFR) p55 and p75 and TNFα concentrations in serum were analyzed before therapy and daily during 8 days of the first therapy cycle. sTNFR was measured by radioimmunoassay. sTNFR p55 increased in all patient groups from a baseline value of 5.2±0.9 ng/ml to a maximum of 13.6±1.2 ng/ml by days 3 – 4 (P = 0.003). sTNFR p75 increased from 7.6±1.1 ng/ml to peak values of 30.1±2.6 ng/ml in groups A and B (P = 0.02). In group C the sTNFR p75 response was weak (NS). In group B, the increase of both p55 and p75 occurred only after addition of IL-2 to IFNα. TNFα increased weakly during treatment with IFNα alone (group B); it rose strongly during IL-2 and the combined treatment (groups A – C) from 8±2 pg/ml to 115±13 pg/ml (P = 0.003). In group  B,  it  reached  the  maximum  24 h  after  addition  of IL-2 to IFNα and decreased thereafter. There was a significant relationship between TNFα and sTNFR p55 or sTNFR p75 in groups A and C, (P = 0.001), but not in group B. Group C was also investigated during the third therapy cycle. The increase of sTNFR p75 was stronger (P = 0.01) and that of TNFα weaker than in the first cycle; the sTNFR p55 response was similar in both cycles. In conclusion sTNFR p55 and p75 are rapidly induced during IL-2 and IL-2+ IFNα treatment, the increase of sTNF receptors parallels or exceeds that of TNFα and may influence the immunomodulatory effects of TNFα during cytokine therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01526206
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Detection of clonally rearranged T-cell-receptor gamma chain genes from T-cell malignancies and acute inflammatory rheumatic disease using PCR amplification, PAGE, and automated analysis (1997)
    Springer
    Annals of hematology 74 (1997), S. 123-130 
    Details
    ISSN: 1432-0584
    Keywords: Key words T-cell malignancies ; PCR ; PAGE ; Automated analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Clonal expansions of T cells carrying identical T-cell-receptor (TCR) genes are the hallmark of T-cell malignancies, but they can also result from a strong immune reaction to a dominant epitope. The basis for the molecular detection of clonal T cells is amplification of the V-(D)-N-J region of the TCR gene. We evaluated PCR amplification of the rearranged gamma TCR from genomic DNA extracted from peripheral blood and subsequent polyacrylamide gel electrophoresis (PAGE) in an automated DNA sequencer. We determined the sensitivity for the detection of clonal T cells and propose a standardized evaluation procedure for the electrophoretic profiles generated by the DNA sequencer. The sensitivity of our method was 0.6–1.25% of clonal T cells within a polyclonal background. Sixteen patients with T-cell malignancies, ten with acute inflammatory rheumatic diseases, and twelve healthy controls were examined. Among the systemic T-cell malignancies, all but one patient with T-PLL (8/9) revealed a clonal PCR signal. No clonal signal was detectable in any patient in clinical complete remission (5/5) or in either of the two patients with lymphomas limited to cutaneous sites. However, clonal T cells were detected in one patient with polymyalgia rheumatica and in one with reactive arthritis. A polyclonal signal was found in the remaining eight patients with acute inflammatory rheumatic diseases and in 12 healthy controls. Taking our results together, the PCR/PAGE assay is able to reliably distinguish clonal from polyclonal T-cell populations. However, although the sensitivity is limited to approximately 1%, clonal T cells can be found in the peripheral blood of some patients with autoimmune diseases and not only in T-cell malignancies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050269
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