Monocyte and Macrophage-Mediated Pathology and Protective Immunity During Schistosomiasis

Infection bySchistosomaparasites culminates in a chronic granulomatous disease characterized by intense tissue fibrosis. Along the course of schistosomiasis, diverse leukocytes are recruited for inflammatory foci. Innate immune cell accumulation in Th2-driven granulomas aroundSchistosomaeggs is associated with increased collagen deposition, while monocytes and macrophages exert critical roles during this process. Monocytes are recruited to damaged tissues from blood, produce TGF-beta and differentiate into monocyte-derived macrophages (MDMs), which become alternatively activated by IL-4/IL-13 signaling via IL-4R alpha (AAMs). AAMs are key players of tissue repair and wound healing in response toSchistosomainfection. Alternative activation of macrophages is characterized by the activation of STAT6 that coordinates the transcription ofArg1, Chi3l3, Relma, andMrc1.In addition to these markers, monocyte-derived AAMs also expressRaldh2andPdl2.AAMs produce high levels of IL-10 and TGF-beta that minimizes tissue damage caused bySchistosomaegg accumulation in tissues. In this review, we provide support to previous findings about the host response toSchistosomainfection reusing public transcriptome data. Importantly, we discuss the role of monocytes and macrophages with emphasis on the mechanisms of alternative macrophage activation during schistosomiasis.