TNFRSF25 and Autoimmunity: 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.