Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review
Adenylate cyclases of Trypanosoma brucei inhibit the innate immune response of the host. / Salmon, Didier; Vanwalleghem, Gilles; Morias, Yannick et al.
In: Science, Vol. 337, No. 6093, 27.07.2012, p. 463-466.Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review
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TY - JOUR
T1 - Adenylate cyclases of Trypanosoma brucei inhibit the innate immune response of the host
AU - Salmon, Didier
AU - Vanwalleghem, Gilles
AU - Morias, Yannick
AU - Denoeud, Julie
AU - Krumbholz, Carsten
AU - Lhommé, Frédéric
AU - Bachmaier, Sabine
AU - Kador, Markus
AU - Gossmann, Jasmin
AU - Dias, Fernando Braga Stehling
AU - De Muylder, Géraldine
AU - Uzureau, Pierrick
AU - Magez, Stefan
AU - Moser, Muriel
AU - De Baetselier, Patrick
AU - Van Den Abbeele, Jan
AU - Beschin, Alain
AU - Boshart, Michael
AU - Pays, Etienne
PY - 2012/7/27
Y1 - 2012/7/27
N2 - The parasite Trypanosoma brucei possesses a large family of transmembrane receptor-like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by about 50% allowed trypanosome growth but reduced the parasite's ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor-α through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.
AB - The parasite Trypanosoma brucei possesses a large family of transmembrane receptor-like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by about 50% allowed trypanosome growth but reduced the parasite's ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor-α through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.
UR - http://www.scopus.com/inward/record.url?scp=84864344932&partnerID=8YFLogxK
U2 - 10.1126/science.1222753
DO - 10.1126/science.1222753
M3 - Journal article
AN - SCOPUS:84864344932
VL - 337
SP - 463
EP - 466
JO - Science
JF - Science
SN - 0036-8075
IS - 6093
ER -