Authors: Jennifer Howard, Séverine Loizon, Christopher Tyler, Dorothée Duluc, Bernhard Moser, Matthieu Méchain, Alexandre Duvignaud, Denis Malvy, Marita Troye-Blomberg, Jean-François Moreau, Matthias Eberl, Odile Mercereau-Puijalon, Julie Déchanet-Merville, Charlotte Behr & Maria Mamani-Matsuda.
Jenny Howard: former PhD student (from 2011 to 2015) in the CNRS UMR5164
Charlotte Behr: group leader (from 2005 to 2013†) in the CNRS UMR5164
Abstract: During Plasmodium falciparum infections, erythrocyte-stage parasites inhibit dendritic cell maturation and function; compromising development of effective anti-malarial adaptive immunity. Human Vγ9Vδ2 T-cells can act in vitro as APCs and induce αβ T-cell activation. However, the relevance of this activity in pathophysiological contexts in vivo has remained elusive. Since Vγ9Vδ2 T-cells are activated during the early immune response against P.falciparum infection, we investigated whether they could contribute to the instruction of adaptive immune responses toward malaria parasites. In P.falciparum-infected patients,Vγ9Vδ2 T-cells presented an increased surface expression of APC-associated markers HLA-DR and CD86. In response to infected red blood cells in vitro, Vγ9Vδ2 T-cells readily up-regulated surface expression of HLA-DR, HLA-ABC, CD40, CD80, CD83 and CD86, induced naive αβ T-cell responses, and cross-presented soluble prototypical protein to antigen-specific CD8+ T-cells. Our findings indicate that P. falciparum parasites induce genuine APC properties in Vγ9Vδ2 T-cells and qualify this subset as an alternative professional APC in malaria patients, which could be harnessed for therapeutic interventions and vaccine design.
Find the publication in advance HERE.