The immune response of dengue fever/dengue hemorrhagic fever is a series of immunopathogenesis processes starting from viral infection to the target on monocytes and macrophages. It may consequently cause a cascade of viremia in the circulation that stimulates the afferent, efferent, and effector mechanism by the interaction of the humoral and complement system. The cascade results in inflammatory substance that will affect capillary permeability and activate coagulation factors leading to further effects on endothelial level. The mechanism involving pathogenesis of DHF/DSS is still vague. So far, a theory of heterologous infection has been developed, which explains that on second infection, there is subneutralization that induce viral replication. The autoimmune mechanism development leads to the better understanding of DHF. It also explains the autoimmune response of the viral infection, which consists of molecular mimicry, bystander activation and viral persistence. The development of the autoimmune pathomechanism is related to the role of autoantibody and endothelial dysfunction that may have role in worsening DHF.