PW assisted with the study fieldwork, participant follow-up and data management, with contributions from GA and SNL. KEB designed and coordinated laboratory testing, which was undertaken by CPM. AJvH advised on the use of study data for cost-effectiveness modelling. All investigators contributed to and approved the final version of the paper. We would like to thank all the families and schools who participated in this study; Teresa Gibbs, Yojna Handoo-Das, Rashmi

Malkani, and Deborah Cohen for administration of the school mailings find more and data entry; Lynne Joslin, Norah Ashwood, Diane Webb, Anne Maher, and Wendy Nedoma, the HPA vaccine research nurses for their assistance in the field work for the study. “
“Since the publication of this paper, the authors have discovered an error in the section ‘Vaccine introduction in low- and middle-income countries’, which they would like to correct. The statement “Among girls attending school, high first dose coverage was achieved (93%) [37]” should read “Among girls attending school, high three-dose coverage was achieved (93%) [37]”.

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“Leishmania lipophosphoglycan (LPG), one of the principal molecules of the parasite, modulates the immune response. LPG is a ligand for TLR2 in NK cells regulating their IFN-γ and TNF-α production [1]. In mast cells and macrophages LPG modulates TLR2 and protein kinase-alpha (PKC-α), respectively [2] and [3]. CD4+ lymphocytes Liothyronine Sodium define Leishmania infections, where a Th-1 aids parasite control and Th-2 response favors disease progression in mouse models [4]. A major role in Angiogenesis inhibitor the defense against Leishmania is played by CD8+ cells, both by IFN-γ production and cytotoxicity [5], [6] and [7]. Activation of CD8+ and CD4+ lymphocytes is regulated by PD-1, an inhibition receptor whose two ligands are PD-L1 (B7-H1) and PD-L2 (B7-DC) [8] and [9]. The recognition of PD-1 by either ligand leads to a functional exhaustion of CD8+ lymphocytes, characterized by reduced proliferation, the absence of cytokine production and a failure

to exert cytotoxicity [10] and [11]. Yet some evidence also suggests that these molecules modulate CD8+ cells during Leishmania mexicana infections. A reduction of CD8+ lymphocytes has been observed in patients with diffuse cutaneous leishmaniasis (DCL), infected with L. mexicana. These cells showed enhanced expression of PD-1 and were hampered in their effectors mechanisms, being non-responsive in their cytokine production and showing limited cytotoxicity, when confronted with autologous Leishmania-infected macrophages [12] and [13]. In a model of experimental chronic visceral leishmaniasis caused by Leishmania donovani, CD8+ cells were found to show phenotypic markers of functional exhaustion [14]. PD-L2 is a ligand for PD-1 displayed on dendritic cells and macrophages, both of which are host cells for Leishmania [9].