Dysregulation of NK cell compartment in lungs of Dp16(1)/Yey mouse model of Down Syndrome: impact of double-stranded RNA mimetic stimulation

DUTTO, JEREMÍAS; ARAYA, PAULA; BOFFELLI, LUCIA; NÚÑEZ NICOLAS GONZALO; ESPINOSA, JOAQUÍN M.; MACCIONI, MARIANA

Congreso; Reunion Anual de Sociedades de Biociencias SAIC SAI-FAIC SAFIS; 2022

Down syndrome (DS) is caused by an extra copy of chromosome (chr) 21. People with DS may experience hyperinflammation during viral infection, which has been associated to the presence of four IFNR genes (Ifnar1, Ifnar2, Ifngr2, Il10rb) in chr21. Here, we use a mouse model of DS, Dp16(1)/Yey (DP16), to analyze the impact of double-stranded RNA mimetics on the innate immune response. DP16 mice have a segmental duplication of a region on murine chr16, syntenic to the portion of chr21 that includes the IFNR genes. DP16 and control mice (n=9) were i.p. injected with the TLR3 ligand poly IC and 15hs later, sacrificed. A 29-parameter spectral flow cytometry characterize innate immune cells within spleen, lung, inguinal lymph nodes (iLN) and mesenteric lymph nodes (mLN). At steady state, the main changes observed were reduced frequencies of cDC1, cDC2, and tDCin spleen (p