These included increased HLA-DR expression (a risk allele for several autoimmune diseases) across all hematopoietic cell lines; MHC-II-mediated antigen presentation (a key mechanism that is dysfunctional in autoimmune diseases) in several processes, including autoimmune diseases and responses to infection; increased neuronal adhesion molecule CNTN2 and increased PD-L1 in T cell–antigen interactions that reduce self-tolerance. This evidence concerns the gene CNTN2 and infection.