The prominent natural susceptibility of CD103+ DCs to virus infection may represent a mechanism that ensures adequate MHC-I Ag presentation in a cytokine milieu dominated by I-IFNs [10], [40], [42] leading to a higher density of peptide-MHC-I complexes on the cell surface facilitated by constant degradation of newly synthesized viral proteins [54], [55], [56], [57]. The gene discussed is ITGAE; the disease is viral infectious disease.