Dataset Information

Murine endometrial and decidual NK1.1+ natural killer cells display a B220+CD11c+ cell surface phenotype.

ABSTRACT: Uterine natural killer (uNK) cells accumulate at the maternal-fetal interface during gestation and are thought to have an important role during pregnancy in both mice and humans. While the cell surface phenotype of human uNK cells is increasingly well defined, less is known regarding the cell surface expression profile of murine uNK cells both before and during gestation. Herein, we demonstrate that murine NK1.1(+) (KLRB1C) endometrial NK (eNK) cells, derived from virgin mice, and NK1.1(+) decidual NK (dNK) cells, obtained from pregnant mice, belong to the B220(+) (PTPRC) CD11c(+) (ITGAX) subset of NK cells. While B220 expression was low on NK1.1(+) eNK cells, it was increased on a subset of NK1.1(+) dNK cells at Embryonic Day 10.5. Endometrial NK and dNK cells also differed somewhat in their expression patterns of two activation markers, namely, CD69 and inducible costimulator (ICOS). The eNK cells acquired a B220(hi)ICOS(+) dNK cell surface phenotype when cultured in vitro in the presence of uterine cells and murine interleukin 15. Thus, the cell surface profiles generated for both NK1.1(+) eNK cells and dNK cells demonstrate that they belong to the recently described B220(+)CD11c(+) subset of NK cells, which are potent cytokine producers.

SUBMITTER: Mallidi TV

PROVIDER: S-EPMC2849826 | biostudies-other | 2009 Aug

REPOSITORIES: biostudies-other

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Murine endometrial and decidual NK1.1+ natural killer cells display a B220+CD11c+ cell surface phenotype.

Mallidi Thomas V TV Craig Laura E LE Schloemann Suzanne R SR Riley Joan K JK

Biology of reproduction 20090415 2

Uterine natural killer (uNK) cells accumulate at the maternal-fetal interface during gestation and are thought to have an important role during pregnancy in both mice and humans. While the cell surface phenotype of human uNK cells is increasingly well defined, less is known regarding the cell surface expression profile of murine uNK cells both before and during gestation. Herein, we demonstrate that murine NK1.1(+) (KLRB1C) endometrial NK (eNK) cells, derived from virgin mice, and NK1.1(+) decid ...[more]

PMID: 19369645

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Project description:Natural Killer (NK) cells have been found to be anergic, exhausted and pro-angiogenic in cancers. NK cell from healthy donors, exposed to TGFβ, acquire the CD56brightCD9+CD49a+ decidual-like-phenotype, together with decreased levels of NKG2D activation marker, increased levels of TIM-3 exhaustion marker, similar to cancer-associated NK cells. Tissue inhibitors of metalloproteases (TIMPs) exert dual roles in cancer. The role of TIMPs in modulating immune cells is a very novel concept, and the present is the first report studying their ability to contrast TGFβ action on NK cells. Here, we investigated the effects of TIMP1 and TIMP2 recombinant proteins in hindering decidual-like markers in NK cells, generated by polarizing cytolytic NK cells with TGFβ. The effects of TIMP1 or TIMP2 on NK cell surface antigens were determined by multicolor flow cytometry. We found that TIMP1 and TIMP2 were effective in interfering with TGFβ induced NK cell polarization towards a decidual-like-phenotype. TIMP1 and TIMP2 counteracted the effect of TGFβ in increasing the percentage of CD56bright, CD16-, CD9+ and CD49a+, and restoring normal levels for TIMP 1 and 2 also inhibited decrease levels of the activation marker NKG2D induced by TGFβ and decreased the TGFβ upregulated exhaustion marker TIM-3. NK cell degranulation capabilities against K562 cells were also decreased by TGFβ and not by TIMP1 or TIMP2. TIMP1 treatment could partially restore degranulation marker CD107a expression. Treatment with recombinant TIMP-1 or TIMP-2 showed a trend, although not statistically significant, to decrease CD49a+ and TIM-3+ expression and increase NKG2D in peripheral blood NK cells exposed to conditioned media from colon cancer cell lines. Our results suggest a potential role of TIMPs in controlling the tumor-associated cytokine TGFβ-induced NK cell polarization. Given the heterogeneity of released factors within the TME, it is clear that TGFβ stimulation represents a model to prove TIMP's new properties, but it cannot be envisaged as a soloist NK cell polarizing agent. Therefore, further studies from the scientific community will help defining TIMPs immunomodulatory activities of NK cells in cancer, and their possible future diagnostic-therapeutic roles.

Dataset Information

Murine endometrial and decidual NK1.1+ natural killer cells display a B220+CD11c+ cell surface phenotype.

Publications

Murine endometrial and decidual NK1.1+ natural killer cells display a B220+CD11c+ cell surface phenotype.

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