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  • Title: Inhibition of term decidual NK cell cytotoxicity by soluble HLA-G1.
    Author: Poehlmann TG, Schaumann A, Busch S, Fitzgerald JS, Aguerre-Girr M, Le Bouteiller P, Schleussner E, Markert UR.
    Journal: Am J Reprod Immunol; 2006; 56(5-6):275-85. PubMed ID: 17076671.
    Abstract:
    OBJECTIVES: Soluble (s)HLA-G1 is produced by trophoblast cells. Aim was to analyze the capacities and mechanisms of sHLA-G1 to regulate interleukin (IL)-2-induced cytotoxicity of natural killer (NK) cells from human deciduas. METHODS: Natural killer cells were isolated from decidual layers of term placentae, stimulated or not with IL-2 and supplemented with various concentrations of recombinant soluble HLA-G1 (sHLA-G1). For NK cell cytotoxicity assays, K562 cells were used as targets. Expression of signal transducer and activator of transcription 3 (STAT3) and perforin was analyzed by Western blotting. Apoptosis was examined by assessment of poly(ADP-ribose) polymerase cleavage. NK cells were analyzed by flow cytometry for IL-2receptor-alpha (IL-2R alpha; CD25) and transferrin receptor CD71 expression. RESULTS: Interleukin-2 increases CD71, STAT3, perforin expression and cytotoxic potential of NK cells. Expression of CD71, STAT3 and perforin decreased simultaneously with cytotoxicity and dose-dependently when sHLA-G1 (1.6 micro g/mL-1.6 ng/mL) was added to IL-2 stimulated cultures. sHLA-G1 did not induce apoptosis and CD25 expression was not affected. CONCLUSION: Interleukin-2R alpha expression is not controlled by sHLA-G1, but its signal transducer STAT3 as well as several downstream effects, such as perforin expression, proliferation and cytotoxicity. The control of STAT3 bioavailability through sHLA-G1 may be a key regulator of the mentioned effects.
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