Mechanisms of this inhibition involved T cell exhaustion and dysfunction, as C3aR-deficiency and blockade reduced the expression T cell inhibitory receptors Pdcd1, Ctla4, and Btla. Depletion of CD8+ T cells entirely abrogated beneficial impact of C3aR-deficiency on tumor growth confirming regulation of T cell function by C3aR (80). Here, CD8A is linked to neoplasm.