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. 2014 Aug;109(5):644–661. doi: 10.1590/0074-0276130597

Fig. 3. : mechanisms of “early-phase” and “late-phase” immunity. Parasite development after traversal of the midgut epithelium is subjected to two “phases” of the mosquito innate immune response. An “early-phase” limits the ookinete survival before or at the transition to oocyst differentiation. As ookinetes traverse the midgut epithelium they undergo nitration (red dots) and in this way are “marked” for immune recognition by complement-like proteins circulating in the mosquito haemolymph [including thioester protein 1 (TEP1)]. Following recognition, TEP1 binds to the ookinete surface to initiate lysis or melanisation that result in parasite killing. A second, “late-phase” immune response limits oocyst survival and involves the production of nitric oxide (NO) by the signal transducer and activator of transcription (STAT) pathway leading to parasite killing. While increased levels of NO have been implicated in this process, it is unclear to what extent the midgut, fat body and possibly haemocytes may contribute to the “late-phase” response. This figure was adapted from Gupta et al. (2009) and Fraiture et al. (2009). APL1: Anopheles Plasmodium-responsive leucine-rich repeat protein 1; BL: basal lamina; LRIM1: leucine-rich immune molecule 1; ME: midgut epithelium; NOS: NO synthase; PM: peritrophic matrix.

Fig. 3