The role of HLA-B in psoriasis immuno-pathogenesis might be similar to that of HLA-C, which has been shown to bind peptide motifs that are shared between the streptococcal M proteins and the wound-healing-associated keratins k16 and k17, thereby clonally expanding the pool of skin-directed autoreactive CD8+ T cells [40]. This evidence concerns the gene KRT17 and psoriasis.