ALT Cross section of olfactory epithelium of ChAT-eGFP mice stained for ChAT-eGFP (tuft cells), cochlin and CFTR (ionocytes), and OMP (olfactory sensory neurons (OSNs), top image). Hoechst (blue) was used to mark nuclei in all images. Green arrows point at tuft cells and magenta arrows point at ionocytes in the top image.

ALT Treating a Primary Immunodeficiency with CRISPR. Familial hemophagocytic lymphohistiocytosis (FHL) is a range of inherited, sometimes fatal, inflammatory diseases caused by loss-of-function mutations in the cytotoxic machinery of immune cells. Li et al. developed an adeno-associated virus (AAV)–based CRISPR–Cas9 system combined with nonhomologous end joining (NHEJ) inhibition to repair memory T cells from perforin (Prf1)-deficient mice as well as from pediatric patients with FHL2 (PRF1 deficiency) or FHL3 (Munc13-4/UNC13D deficiency). Repaired mouse T cells could then prevent or cure FHL2-like disease in Prf1-knockout mice triggered by Epstein–Barr virus (EBV)–driven B cell hyperproliferation. This month’s cover illustration depicts CRISPR–Cas9–mediated repair of a cytotoxic T cell (red), which allows it to secrete normal cytotoxic granules (pink) and effectively kill virally infected B cells (blue).

ALT tSNE plot showing 35 clusters of thymic non–T hematopoietic cells, based on 10x Genomics scRNA-seq data, combined from thymi of WT male mice treated with Dex 4 days or 18 hours before and untreated controls. N = 2 animals. Black font indicates the proposed cell type classification of the corresponding clusters.