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  • CA1  (1)
  • CD56  (1)
  • CD8  (1)
  • Histiocytic necrotizing lymphadenitis  (1)
  • Ischemia  (1)
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  • 1
    ISSN: 1432-2307
    Schlagwort(e): Key words TIA-1 ; CTL ; Apoptosis ; Histiocytic necrotizing lymphadenitis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  Cell death is necrotic or apoptotic. In histiocytic necrotizing lymphadenitis (HNL), apoptosis is the main form of cell death, resulting in the creation of nuclear debris that is one of the characteristic features of HNL. To investigate the cell type of apoptotic cells, 12 cases of HNL were analyzed using the immunohistochemical staining for TIA-1, a cytotoxic granule of either cytotoxic T or NK cells. One quarter to over half of all apoptotic cells were positive for TIA-1, and some of the nuclear debris was also positive. The necrotic lesions of HNL were found to consist of nuclear debris, apoptotic cells, histiocytes and lymphocytes. The lymphocytes were mainly CD8-positive T-cells or CD4-positive cells, while B- and NK cells were only rarely observed. The number of TIA-1-positive lymphocytes was more closely related to the number of CD8-positive cells than to the number of CD4 cells. In double staining, the TIA-1 positive lymphocytes were mainly CD8 positive, but rarely CD4 positive. In HNL, then, CD8-positive cytotoxic T-cells are likely to undergo apoptosis.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-1106
    Schlagwort(e): Key words F3/contactin ; Ischemia ; Hippocampus ; CA1 ; Sprouting ; Gerbil
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  We studied changes in expression of F3/contactin (F3), a neuron-specific adhesion molecule, in the gerbil hippocampus after transient forebrain ischemia for 5 min. By immunohistochemical techniques using F3 antibody, we found a biphasic change in immunoreactivity for F3 in the CA1 area after ischemia. Western blotting of F3 protein showed a similar biphasic change. F3 immunoblots decreased to 67% of the control at 1 week, but then they increased and attained 159% at 3 weeks and 152% at 5 weeks after ischemia. Immunoreactivity of a neurofilament (NF145) showed a similar biphasic change to F3 but to a lesser extent. In contrast, microtubule-associated protein 2 (MAP2) immunoreactivity uniformly decreased after ischemia. In situ hybridization revealed that F3 messenger RNA (mRNA) hybridization signals in CA1 area were greatly reduced 1 week after ischemia, while the signals in the CA3 area were unchanged and even increased 3 weeks after ischemia. Damage to CA3 neurons by hyperthermic ischemia blocked the F3 increase in area CA1. Our results suggest that the initial decrease in F3 following ischemia reflects loss of CA1 neurons and the late increase in F3, which shows that a similar time course with neurofilaments may be caused by neurite sprouting.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-2307
    Schlagwort(e): Key words ATLL ; CD8 ; CD56 ; Cytotoxic molecules
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  Adult T-cell leukaemia/lymphoma (ATLL) cells usually exhibit a CD4+ (helper/inducer) phenotype (CD4+/8–/56–), and only a minority of tumours express the CD8 (cytotoxic/suppressor) or CD56 (natural killer [NK]-associated) antigens. TIA-1 is a cytotoxic granule-associated protein expressed in NK cells and cytotoxic T lymphocytes (CTLs). Granzyme B, perforin and Fas ligand (FasL) are also expressed in activated CTLs and NK cells. To clarify the cytotoxic potential of ATLL cells, immunohistochemistry was performed in CD8+ and/or CD56+ ATLL cells, using anti-TIA-1, anti-granzyme B, anti-perforin and anti-FasL antibodies. We studied nine cases of CD8+ and/or CD56+ ATLL, all of which exhibited monoclonal integration of human T-cell leukaemia virus type 1 (HTLV-1) proviral DNA. Four cases exhibited a CD8+/CD56– phenotype, four others had a CD8–/CD56+ phenotype, and one was CD8+/CD56+. All but one case also expressed the surface antigens CD3, TCR αβ, and CD4. Expression of granzyme B and TIA-1 were demonstrated in three and two cases, respectively, but none expressed perforin or FasL. In the control study, 10 cases with typical CD3+/4+/8–/56– ATLL demonstrated no expression of those cytotoxic-associated proteins. Our findings suggest that CD8 and/or CD56 positivity probably confer(s) no cytotoxic function on ATLL cells, and it is possible that CD8 and CD56 may be simply aberrant surface markers in ATLL.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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