Authors declare no conflict of interest. H.S researched the data, performed the experiments, analysed and wrote the manuscript. Å.L recruited the patients, researched the data, reviewed and edited the manuscript. F.V-S researched the data, reviewed and edited the manuscript. “
“The transmission of scabies occurs with the burrowing of Sarcoptes scabiei var. hominis mites into the skin. Infestation invariably Rucaparib order leads

to the development of localized cutaneous inflammation, pruritis and skin lesions. Classical transmission studies document an initial increase in S. scabiei numbers subsequent to primary infestation with a gradual reduction as host immunity develops. However, certain individuals fail to Trametinib research buy control infection and develop severe crusting of the skin, accompanied with extremely high mite burdens, elevated antibody levels and eosinophilia. These individuals have the nonhealing form of the human disease known as crusted scabies. The genetic predisposition for susceptibility or resistance to S. scabiei infection in humans is hypothesized to correlate with the dominance of an IgE-driven Th2 response in severe disease or

an interferon-γ-dominated Th1 response that promotes parasite control. However, recent data reveals complexities in cytokine regulation in the skin and the mechanisms of acquired resistance and immune escape. In this review, we consider the recent immunological and biomolecular advances

in understanding the human host immune response to S. scabiei infestations in the context of earlier studies and attempt to reconcile apparent differences and emphasize those aspects of the Th1/Th2 model that are supported or refined. Human responses to parasitic infections have often been difficult to define as either Th1 or Th2, as characteristics from both response types are often reported (1). However, there is accumulating evidence that the host immune response GBA3 to crusted scabies resembles a nonprotective Th2 allergic response, and ordinary scabies resembles a Th1 cell-mediated protective response (2–5). Th1-biased immune reactions are dominated by CD4+ and CD8+ T cells secreting IFN-γ and IL-2 (6). Th2-biased T cells (secreting net IL-4, IL-5 and IL-13) are dominant effector cells in the pathogenesis of IgE-mediated hypersensitivity including attracting, activating and prolonging the survival of nonspecific effector cells. The Th1/Th2 concept has also been extended to T-regulatory populations expressing IL-10 and transforming growth factor-β (TGF-β).