Pregled bibliografske jedinice broj: 484121
Galectin-3 deletion modulate NK cell activation
Galectin-3 deletion modulate NK cell activation // 12th meeting of the Society for Natural Immunity and NK : Book of abstracts / Jonjić, Stipan ; Krmpotić, Astrid ; Watzl, Carsten (ur.).
Rijeka, 2010. str. 122-122 (poster, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 484121 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Galectin-3 deletion modulate NK cell activation
Autori
Radosavljević, Gordana ; Mitrović, Maja ; Jovanović, Ivan ; Juranić Lisnić, Vanda ; Arsenijević, Nebojša ; Jonjić, Stipan ; Krmpotić, Astrid ; Hsu, Daniel ; Lukić, Miodrag
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
12th meeting of the Society for Natural Immunity and NK : Book of abstracts
/ Jonjić, Stipan ; Krmpotić, Astrid ; Watzl, Carsten - Rijeka, 2010, 122-122
Skup
Mmeeting of the Society for Natural Immunity and NK (12 ; 2010)
Mjesto i datum
Cavtat, Hrvatska, 11.09.2010. - 15.09.2010
Vrsta sudjelovanja
Poster
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
galectin-3; NK cell
Sažetak
Galectin-3, a β-galactoside binding protein with immune regulatory functions, is overexpressed in a variety of tumor and immune cells in response to various stimuli. Although the expression of Galectin-3 on uterine NK cells (uNK cells) has been suggested to downregulate their function, little is known about the role of Galectin-3 on NK cells, in general. We have observed recently, that Galectin-3-deficient (Gal-3-/-) mice are more resistant to metastatic malignant melanoma. NK cells have been shown critical in reducing tumor lung metastases in melanoma. Objectives: We have investigated the number and phenotype of spleen NK cells in Gal-3-/- and "wild type" (WT) C57BL/6 mice. Methods: We used female Gal-3-/- C57BL/6 and WT C57BL/6 mice, aged 11 weeks. Single-cell suspensions of splenocytes were incubated with mAbs specific for mouse CD3, CD19, NK1.1, CD27, CD11b, and KLRG1, or isotype-matched controls and analised by FACSAria Flow cytometer. Results: Galectin-3-deficient mice have a lower total number of CD3-NK1.1+ cells derived from spleen compared to WT mice (p=0, 008). Despite the reduction in total CD3-NK1.1+, Gal-3-/- mice have a significantly higher percentage of effective cytotoxic and cytokines-producing CD27highCD11bhigh NK cells (p=0, 001) as well as the percentage of immature CD27lowCD11bhigh NK cells (p=0, 004) compared to WT control mice. In contrast, CD27lowCD11bhigh less responsive NK cells were more numerous in Gal-3+/+ mice (p=0, 001). Remarkably, we noticed significantly lower percentage of KLRG1 receptor on NK cells of Gal-3-/- mice as compared to WT control mice (p=0, 002). As KLRG1 is expressed on CD27lowCD11bhigh NK cells, this finding is in accordance with our previous observation. Conclusion: Our data suggest that Galectin-3-deficient mice constitutively have a significantly higher percentage of effective cytotoxic and immature NK cells and this might indicate that gal-3-/- mice display faster turnover of NK cells than WT control mice. These results support our previous findings that lack of Galectin-3 renders mice resistant to lung metastases and enhance innate cytotoxicity in malignant melanoma.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Ustanove:
Medicinski fakultet, Rijeka
Profili:
Vanda Juranić Lisnić
(autor)
Astrid Krmpotić
(autor)
Maja Arapović
(autor)
Stipan Jonjić
(autor)