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  • 1
    Electronic Resource
    Electronic Resource
    Engagement of MHC Class I Proteins on Natural Killer Cells Inhibits their Killing Capacity (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: We have studied whether engagement of MHC class I (MHC—I) molecules on natural killer (NK) cells can influence the NK killing activity. Human NK effector cells, enriched by nylon wool passage, were incubated with monoclonal antibodies (MoAb) to MHC—I followed by cross-linking with secondary rabbit anti mouse Ig or streptavidin. Cross linking of MHC—I molecules on NK cells resulted in a clear inhibition of the NK activity against the target cells K562, Molt-4 and U937. The inhibitory effect was selective for MHC—I and was not seen with MoAb to MHC—II or CD56 molecules. The inhibition was not mediated via Fc receptors since F(ab)2 fragments of the MHC—I MoAb W6/32 were as effective as the intact antibody. The best inhibition of NK activity was obtained using biotin-labelled F(ab)2 fragments of W6/32 and streptavidin as a cross-linker, where up to 70 % reduction in NK cell activity was observed. Antibody dependent cellular cytotoxicity (ADCC) was also inhibited by cross-linking MHC—I molecules on the effector cells.The results show that antibody mediated cross-linking of MHC—I proteins on NK cells can inhibit their killing capacity. This indicates that MHC—I molecules on NK cells can be involved in the regulation of NK cytotoxicity, perhaps by transmitting inhibitory signals into the NK cell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1995.tb03622.x
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  • 2
    Electronic Resource
    Electronic Resource
    Synovial Cells Responding to a 65-kDa Mycobacterial Heat Shock Protein have a High Proportion of a TcRγδ Subtype Uncommon in Peripheral Blood (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 32 (1990), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have analysed the ability of T cells from synovial fluid mononuclear cells (SFMC) and from peripheral blood mononuclear cells (PBMC) of inflammatory arthritic diseases to proliferate in response to mycobacterial antigens (65-kDa heal shock protein [hsp] of BCG. whole BCG) and to rat collagen type II. The SFMC demonstrated a significantly greater ability to respond to 65-kDa hsp of BCG. and to whole BCG, compared with PBMC from the same patients, With collagen type II, only a small proportion of the patients showed a proliferative response, although with this antigen also SFMC responded better than PBMC. There was no difference between SFMC and PBMC in the response to control antigen (tetanus toxoid), phytohaemagglutinin (PHA), or interleukin 2 (IL-2). A high proportion of cells in SFMC-derived short-term T-cell lines were of TcRγδ type, often exceeding the number of TcRγδ type. There was a significantly higher proportion of TcRγδ cells in the SFMC lines compared with the PBMC lines, and a large part of the TcRγδ cells in she SFMC cultures was CD8+ The SFMC lines had a high proportion of δ- TCS-1+ cells (Vδ1) among their TcRγδ cells, always exceeding the percentages of TiγA+ (Vγ9) and BB3+ (Vδ2) in the PBMC lines, the distribution of TcRγδ subtypes was markedly different, with a TiγA+/BB3+ population in the majority. These data argue for a different subpopulation distribution of TcRγδ cells in synovial fluid compared with peripheral blood of patients with inflammatory arthritic diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1990.tb03191.x
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  • 3
    Electronic Resource
    Electronic Resource
    Human MHC Class I Antigens are Associated with a 90-kDa Cell Surface Protein (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 34 (1991), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Human MHC class I proteins are expressed on almost all nucleated cells as a heavy chain (about 45 kDa) non-covalently associated with β-microglobulin (12 kDa), In this report we show that MHC class I (MHC-I) proteins can also be associated with a 90-kDa protein in the cell membrane.Surface-radiolabelled cells were treated with dithiobis succinimidyl propionate (DSP) in order to preserve multimer protein complexes during cell lysis. The lysates were immunoprecipitated and analysed by SDS-PAGE and autoradiography, Immunoprecipitation of human MH C- I proteins co-precipitated another protein of about 90 kDa in molecular weight p90. p90wasco-precipitaled from all the MIIC-I expressing cells tested: WIT. Raji. Molt-4 and IFN-γ treated K562, but not from untreated, MHC-I negative K562. A 90-kDa protein was also co-precipitated with MHC-I from fresh peripheral blood mononueiear cells(PBMC). Furthermore, p90 was co-precipitated by different MoAbs lo the MHC-1 heavy chain or β2-microglobulin. bul not by control antibodies. Two additional co-precipitaling proteins al 34 kDa and 28 kDa were seen in MHC-I precipitates from Raji cells.Our results suggest that MHC-1 proteins and the 90-kDa protein are associated in the cell membrane, probably by a close but weak, non-covalent interaction. Two additional cell surface proteins at 34 kDa and 28 kDa seem to be MHC-I associated on Raji Burkitt's lymphoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1991.tb01540.x
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  • 4
    Electronic Resource
    Electronic Resource
    Characterization of T-Cell Receptor αβ Repertoire in Synovial Tissue from Different Temporal Phases of Rheumatoid Arthritis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 35 (1992), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: With the aim of investigating the distribution of T cells expressing different T-cell receptors (TCR) in the inflamed synovial tissue of rheumatoid arthritis patients, we have used the polymerase chain reaction to amplify TCR Vα and Vβ transcripts from synovial biopsies obtained by arthroscopy from patients with arthritis of variable duration. From each of nine patients a single biopsy was taken. Southern hybridization analysis of amplified products revealed extensive heterogeneity of TCR Vβ in most patients. On the other hand, restriction in Vα gene expression was seen in several patients. A highly restricted Vα repertoire was observed in all cases with arthritis of short duration. In addition, two of three samples of short duration yielded a more limited number of Vβ transcripts than the others. No conformity was, however, seen in usage of individual Vα and Vβ transcripts among the investigated patients. The present data thus demonstrate variability in synovial TCR expression between rheumatoid arthritis patients, but they also indicate a development towards greater diversity with increasing disease duration, implicating the necessity for careful choice of cases, preferentially selecting for early stages of disease, when further analysing rheumatoid synovial T cells for TCR usage as well as for antigen specificity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1992.tb02846.x
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  • 5
    Electronic Resource
    Electronic Resource
    Dextran sulfate sodium (DSS) induced experimental colitis in immunodeficient mice: Effects in CD4+-cell depleted, athymic and NK-cell depleted SCID mice (1996)
    Springer
    Inflammation research 45 (1996), S. 181-191 
    Details
    ISSN: 1420-908X
    Keywords: Disease models ; Mice ; Immunocompromised ; Ulcerative colitis ; Dextran sulfate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Administration of dextran sulfate to mice, given in the drinking water results in acute or subacute colonic inflammation, depending on the administration protocol. This colonic inflammation exhibits ulceration, healing and repair, and a therapeutic response that makes it valuable for the study of mechanisms that could act in the pathogenesis of human ulcerative colitis, a disease thought to have an immunologically dependent pathogenesis. To investigate if immunological mechanisms were involved in the induction of colonic inflammation in this model, mice with different degrees of immunodeficiency were used. It was shown that dextran sulfate induced colitis could be induced in Balb/c mice depleted of CD4+ helper T cells by treatment with monoclonal antibodies preceded by adult thymectomy. The depletion of CD4+ was verified by flow cytometric analysis. Furthermore, the colonic inflammation could equally be induced in athymic CD-1 nu/nu mice lacking thymusderived T cells, in T and B-cell deficient SCID mice, and also in SCID mice depleted of NK cells by treatment with anti-asialo GM1 antibodies. The NK-cell depletion was verified by measuring spleen NK-cell activity. The resulting colonic inflammation in all these types of deficient mice was qualitatively comparable, as shown by clinical and histological appearance. These results indicate that the presence of functional T, B and NK cells is not crucial for the induction of dextran sulfate colitis in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02285159
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