Subversion of Immunity by Leishmania amazonensis Parasites: Possible Role of
Phosphatidylserine as a Main Regulator
Figure 1
PS exposure on intracellular amastigotes of L. amazonensis: hypothesis for T-cell-dependent modulation. T cells primed by leishmanial antigens display a pathogenic phenotype, characterized by the production of unpolarized cytokines [18, 31]. These cytokines are able to activate both iNOS- and arginase 1-dependent intracellular macrophage pathways (Wanderley, JL et al. unpublished). In this environment, amastigotes receive stress from iNOS-derived nitric oxide (NO) which triggers high levels of surface PS on the parasite (Wanderley, JL et al. unpublished). Simultaneously, arginase 1 is also induced, and the outcome of this activation is an increase in polyamine intracellular levels [65]. Polyamines are indispensable for parasite survival and proliferation, maintaining them even in the presence of NO (Wanderley, JL et al. unpublished, [63]). Upon macrophage disruption, highly infective PSHIGH amastigotes are released, being capable of infecting new host cells and of spreading the anti-inflammatory signals derived from PS recognition (dashed arrow). PV: parasitophorous vacuole, ODC: ornithine decarboxylase, iNOS: inducible nitric oxide synthase, M: macrophage, Am: amastigote.
