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Helminths cause chronic infections and affect the immune response to unrelated inflammatory diseases. Although helminths have been used therapeutically to ameliorate inflammatory conditions, their anti-inflammatory properties are poorly understood. Alternatively activated macrophages (AAMϕs) have been suggested as the anti-inflammatory effector cells during helminth infections. Here, we define the origin of AAMϕs during infection with  Taenia crassiceps , and their disease-modulating activity on the Experimental Autoimmune Encephalomyelitis (EAE). Our data show two distinct populations of AAMϕs, based on the expression of PD-L1 and PD-L2 molecules, resulting upon  T. crassiceps  infection. Adoptive transfer of Ly6C +  monocytes gave rise to PD-L1 + /PD-L2 + , but not PD-L1 + /PD-L2 −  cells in  T. crassiceps -infected mice, demonstrating that the PD-L1 + /PD-L2 +  subpopulation of AAMϕs originates from blood monocytes. Furthermore, adoptive transfer of PD-L1 + /PD-L2 +  AAMϕs into EAE induced mice reduced disease incidence, delayed disease onset, and diminished the clinical disability, indicating the critical role of these cells in the regulation of autoimmune disorders.

Helminth-induced Ly6Chi monocyte-derived alternatively activated macrophages suppress experimental autoimmune encephalomyelitis