Amongst T-cell and monocytes/macrophages, some immune-stimulatory or auto-regulatory interactions were seen (CTLA4 or CD28/CD80 or CD86, CCL5/CCR5) (Fig. 8f), but specific epithelial to T-cell interactions in critical COVID-19 were limited to pro-inflammatory ICAM1-mediated interactions (Fig. 8g). This evidence concerns the gene CD28 and COVID-19.