Coincidental Loss of DOCK8 Function in NLRP10-Deficient and C3H/HeJ Mice Results in Defective Dendritic Cell Migration

Jayendra Kumar Krishnaswamy
Arpita Singh
Uthaman Gowthaman
Renee Wu

Jayendra Kumar Krishnaswamy;Arpita Singh;Uthaman Gowthaman;Renee Wu;Pavane Gorrepati;Manuela Sales Nascimento;Antonia Gallman;Dong Liu;Anne Marie Rhebergen;Samuele Calabro;Lan Xu;Patricia Ranney;Anuj Srivastava;Matthew Ranson;James Gorham;Zachary McCaw;Steven Kleeberger;Leonhard Heinz;André C. Müller;Keiryn Bennett;Giulio Superti-Furga;Jorge Henao-Mejia;Fayyaz Sutterwala;Adam Williams;Richard Flavell;Stephanie Eisenbarth


Understanding dendritic cell (DC) migration during an immune response is fundamental to defining the rules that govern T cell-mediated immunity. We recently described mice deficient in the pattern recognition receptor NLRP10 (NLR family, pyrin domain containing 10) with a severe DC migration defect. Using whole-exome sequencing, we discovered that this defect was due to mutation of the guanine nucleotide exchange factor Dock8 (dedicator of cytokinesis 8). DOCK8 regulates cytoskeleton dynamics in