Open Accessp47 licenses activation of the immune deficiency pathway in the tick Ixodes scapularis
Author(s) -
Erin E. McClure Carroll,
Xiaowei Wang,
Dana K. Shaw,
Anya J. O’Neal,
Adela S. Oliva Chávez,
Lindsey J. Brown,
Vishant Mahendra Boradia,
Holly Hammond,
Joao H. F. Pedra
Publication year - 2018
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1808905116
Subject(s) - ixodes scapularis , biology , borrelia burgdorferi , xiap , inhibitor of apoptosis , jurkat cells , ixodes , immune system , tick , microbiology and biotechnology , virology , genetics , t cell , programmed cell death , apoptosis , caspase , antibody
Significance Translocation of the nuclear factor (NF)-κB homolog Relish in response to microbial infection is a hallmark of the arthropod immune deficiency (IMD) pathway. Classically, transduction within the IMD molecular cascade is regulated by the inhibitor of apoptosis protein 2 (IAP2). In the Lyme diseaseIxodes scapularis tick, X-linked inhibitor of apoptosis (XIAP) is considered a functionally analogous enzyme. Ticks lack homologs for some genes of the IMD network. As such, substrates of XIAP remain elusive. Here, we identify the molecule p47 as a binding partner of XIAP and Kenny (IKKγ/NEMO). We demonstrate that p47 induces a signaling cascade within the tick IMD pathway to limit microbial infection. This work emphasizes the importance of studying ticks to discover fundamental immunological processes.
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