Specifically, they suggest that, beside the traditional alterations in immune check points of B cell tolerance and in the antigen presentation of self-antigen by HLA alleles associated to higher risk to develop autoimmunity, such the HLA-B27 in Reactive Arthritis and DR3 and DRB1 in Systemic lupus erythematosus (SLE), genetic susceptibility may lead to abnormally strong reactions to bacterial curli. This evidence concerns the gene TNFRSF25 and systemic lupus erythematosus.