Figure 3
Human endogenous retroviruses and their hypothetical role in psoriasis. During HIV-1 infection, HIV-1 tat protein acts as a trans-acting factor activating HERV's long terminal repeat (LTR). Stimulation of the trans-activation region (TAR) by its interaction with the HIV-1 tat protein activates transcription. Subsequently, exogenous retroviruses trigger an immune response, and HERV-encoded proteins are recognized as self-antigens (molecular mimicry) awakening a cellular-based autoimmune phenomenon.