On this basis, Hill and co-workers proposed for the first time that DRB1 alleles with the common epitope can elicit an autoimmune response to citrullinated RA antigens due to a significant increase in MHC-peptide interaction accompanied by an activated CD4+ T-cell response in HLA-DRB*0401 transgenic mice [100]. The gene discussed is CD4; the disease is rheumatoid arthritis.