Some examples include data on Th17 cells, cytokines, or other mediators variably involved in the autoimmunity mechanisms such as BLIMP-1, IL-10, IFN, or NF-kB.
Gene-function studies have revealed mechanisms through which SLE-associated alleles of IFIH1, TNFAIP3, IRF5, and PRDM1 likely contribute to the development of autoimmunity.
Hence, these data identified ectopic Blimp1 expression as a novel mechanism, through which Blimp1 can act as a risk factor in the development of autoimmune disease.
Gene-function studies have revealed mechanisms through which SLE-associated alleles of IFIH1, TNFAIP3, IRF5, and PRDM1 likely contribute to the development of autoimmunity.
PRDM1 expression has not been shown to display gender-differential thymic expression, but its expression level and its gene polymorphisms are associated with female-dependent autoimmune disease risk.
Blimp-1 also functions as a gatekeeper of T cell activation and suppression to prevent or dampen autoimmune disease, antiviral responses and antitumor immunity.
Thus, Blimp-1 deficiency in DCs led to loss of appropriate regulation of Ctss expression in female mice and thereby modulated antigen presentation and the T<sub>FH</sub> cell repertoire to contribute to autoimmunity.
In this review, we will discuss the immune regulatory functions of Blimp-1 in DCs with a main focus on the tolerogenic mechanisms of Blimp-1 required to protect against the development of autoimmune diseases.