Clinical and immunological spectra of human cutaneous leishmaniasis in North Africa and French Guiana.

Cutaneous leishmaniasis (CL) caused by infection with the parasite exhibits a large spectrum of clinical manifestations ranging from single healing to severe chronic lesions with the manifestation of resistance or not to treatment. Depending on the specie and multiple environmental parameters, the evolution of lesions is determined by a complex interaction between parasite factors and the early immune responses triggered, including innate and adaptive mechanisms. Moreover, lesion resolution requires parasite control as well as modulation of the pathologic local inflammation responses and the initiation of wound healing responses.

Autophagy Pathways in the Genesis of -Derived Microvesicles: A Double-Edged Sword?

Malaria, caused by species (spp.), is a deadly parasitic disease that results in approximately 400,000 deaths per year globally. Autophagy pathways play a fundamental role in the developmental stages of the parasite within the mammalian host.

Consistent concentrations of critically endangered Balearic shearwaters in UK waters revealed by at-sea surveys.

Aim: Europe's only globally critically endangered seabird, the Balearic shearwater (), is thought to have expanded its postbreeding range northwards into UK waters, though its at sea distribution there is not yet well understood. This study aims to identify environmental factors associated with the species' presence, map the probability of presence of the species across the western English Channel and southern Celtic Sea, and estimate the number of individuals in this area.

Location: The western English Channel and southern Celtic Sea.

Uses a TLR3-Dependent Pathway to Achieve Mammalian Host Parasitism.

Malaria is associated with complicated immunopathogenesis. In this study, we provide evidence for an unexpected role of TLR3 in promoting the establishment of infection through delayed clearance of parasitemia in wild type C57BL/6jRj (B6) compared with TLR3 knockout mice. In this study, we confirmed an increased expression of , , , and in the liver 42 h postinfection and the initiation of an early burst of proinflammatory response such as , , and in B6 mice that may promote parasite fitness.