Fig. 1

Current knowledge on immune mechanisms in scabies: The figure shows possible mechanisms of immune responses to scabies mite infestation. Keratinocytes, langerhans cells, and macrophages in the skin respond to mite antigens, secreting proinflammatory cytokines such as TNF-α, IFN-γ, TGF-β, IL-1β and IL-23. This leads to the differentiation and recruitment of CD8⁺ T and CD4⁺ Th1 and Th2 cells into the skin. Secreted cytokine milieus of IL-6, TGFβ and IL-23 promote the differentiation of Th17 or Tc17 cells and IL-17 production. IL-23 and IL-1β also have firmly established roles in promoting IL-17 production by γδ T cells, and their increased expression observed in CS may act in an amplification loop for IL-17 production, promoting inflammation and aggravating immune pathology. TGF-β and IL-2 induce Tregs. IL-10 and TGF-β production by Tregs may contribute to the delayed inflammatory response in scabies and suppress pathological inflammation in ordinary scabies, regulating innate and adaptive responses. Immune responses to ordinary scabies appear Th1 oriented as evidenced by strong IFN-γ secretion in response to mite antigens. Increased expression of the Th2 cytokines IL-4 and IL-3 in CS leads to immunoglobulin switching in B cells resulting in secretion of large amounts of IgE and IgG. IL-5 activates and promotes the maturation of eosinophils at the site of infestation, sustaining the local Th2 inflammatory responses. IgE through its high affinity receptor (FcεRI) activates mast cells. These cells produce inflammatory mediators such as TNF, histamine, leukotrienes, IL-4, IL-5 and IL-13, supporting their contribution to allergic inflammation in CS. Cells highlighted in “red” and with “?” are not yet defined in scabies