Leishmaniasis is a vector-borne neglected tropical disease that affects more than 700,000 people annually. Leishmania parasites cause the disease, and different species trigger a distinct immune response and clinical manifestations. Macrophages are the final host cells for the proliferation of Leishmania parasites, and these cells are the key to a controlled or exacerbated response that culminates in clinical manifestations. M1 and M2 are the two main macrophage phenotypes. M1 is a pro-inflammatory subtype with microbicidal properties, and M2, or alternatively activated, is an anti-inflammatory/regulatory subtype that is related to inflammation resolution and tissue repair. The present review elucidates the roles of M1 and M2 polarization in leishmaniasis and highlights the role of the salivary components of the vector and the action of the parasite in the macrophage plasticity.

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Infection with dengue virus (DENV) can lead to a wide spectrum of clinical presentations, ranging from asymptomatic infection to death. It is estimated that the disease manifests only in 90 million cases out of the total 390 million yearly infections. Even though research has not yet elucidated which are the precise pathophysiological mechanisms that trigger severe forms of dengue, the infection elicits a critical immune response significant for dengue pathogenesis development. Understanding how the immune response to DENV is established and how it can resolve the infection or turn into an immunopathology is of great importance in DENV research. Currently, studies have extensively debated 2 hypotheses involving immune response: antibody-dependent enhancement and cytokine storm. However, despite its undeniable importance in severe forms of the disease, these 2 hypotheses are based on a primed immune status resulting from previous heterologous infection, abstaining them from explaining the severe forms of dengue in naive immune subjects, for example. Thus, it seems that a more intricate arrangement of causes and conditions must be achieved to severe dengue to occur. Among them, the cytokine network signature elicited, in association with viral aspects deserves special attention regarding the establishment of infection and evolution to pathogenesis. In this work, we intend to shed light on how those elements contribute to severe dengue development.