High expression of co-inhibitory receptors, e.g., PD1, is a hallmark of exhausted T cells,37 and blockade of PD1 increases the function of exhausted CD8+ T cells.38,39 Interestingly, CD47 has also been found to be upregulated as an early host response to infection, and mice treated with anti-CD47 monoclonal antibody showed enhanced DC activation and CD8+ T cell response to chronic viral infection.40 Therefore, understanding the role of CD47 in CD8+ T cell activation, proliferation, and exhaustion is important for designing CD47-targeted immunotherapeutics. Here, CD8A is linked to infection.