Galectin-9 influences the Tim-3 molecule expression in natural killer different subpopulations
نویسندگان
چکیده
Galectin-9 is a b-galactoside binding lectin with expressed immunoregulatory activity. During pregnancy galectin-9 produced by trophoblast cells and regulates the function of natural killer (NK) at maternal-fetal interface via to Tim-3 (T-cell Ig mucin domain-containing protein 3) molecules. Natural lymphocytes belong innate lymphoid cells, which have cytotoxic effect on target are capable producing large number regulatory factors (cytokines, chemokines). Decidual NK tolerant phenotype play leading role in regulation invasive growth provide peripheral immune tolerance area uteroplacental contact. Peripheral express concentration increased blood during physiologic pregnancy. At functions changed maintain maternal–fetal tolerance. migrate transformed into decidual NK-like cells. decreased women complicated miscarriage. However effects different cell subpopulations not investigated. Therefore, we studied influence transformation expression isolated from healthy non-pregnant fertile women. CD56 + were obtained immunomagnetic separation cultivated vitro 72 hours cytokines (IL-2 IL-15). (5 ng/mL) anti-Tim-3 (10 mg) antibodies added cultures. corresponded its level first trimester The (CD16 - bright ), dim/- ) assessed flow cytometry. It was found that all NK, CD16 dim NK). Incubation did change reduced percentage culture, but Thus, molecule subpopulation distributions culture.
منابع مشابه
Tim-3 is an inducible human natural killer cell receptor that enhances interferon gamma production in response to galectin-9.
NK-cell function is regulated by the integration of signals received from activating and inhibitory receptors. Here we show that a novel immune receptor, T-cell Ig and mucin-containing domain-3 (Tim-3), is expressed on resting human NK cells and is up-regulated on activation. The NK92 NK-cell line engineered to overexpress Tim-3 showed a marked increase in IFN-γ production in the presence of so...
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ژورنال
عنوان ژورنال: ??????????? ???????????
سال: 2023
ISSN: ['2409-5788']
DOI: https://doi.org/10.15789/1563-0625-git-2778