|Number of samples:||7|
|Release date:||Jun 13 2016|
|Last update date:||Oct 24 2018|
|Diseases:||Deficiency Diseases, Neoplasms|
|Genes:||DICER1, ITGAX, MRC1, IFNG, STAT1, TRIM63, PDCD1|
|Dataset link||DICER controls macrophage polarization and tumor response to immunotherapy|
To explore the role of DICER in the development, activation and immunological functions of TAMs, we crossed homozygous LysM-Cre (Clausen et al., 1999) with Dicerlox/lox (Harfe et al., 2005) mice to obtain mice with myeloid-cell-specific Dicer1 gene deletion (LysM-Cre;Dicer–/–, referred to as D–/–). These mice were then backcrossed to LysM-Cre to obtain the control LysM-Cre; Dicer+/+ mice (referred to as D+/+). Both LysM-Cre and Dicerlox/lox mutations were always homozygous in our experiment. We then inoculated Lewis lung carcinoma (LLC) cells subcutaneously (s.c.) in D–/– and control D+/+ mice. Once the tumors were established, we isolated by fluorescence-activated cell sorting (FACS) tumor-associated macrophages (F4/80+ cells).