GSE211109
Transcriptomic profile of neutrophils and macrophages from APLAID mutant mice
Missense mutations in the PLCg2 gene can cause autoinflammation, antibody deficiency and immune dysregulation (APLAID). Clinical and laboratory features include recurrent blistering skin lesions, pulmonary manifestations, inflammatory eye – and bowel diseases accompanied by reduced class-switching memory B cell counts and recurrent infections. Disease onset occurs typically during childhood with varying degrees of severity. To date there is no known cure of APLAID. The potential mechanism by which autoinflammation is promoted in APLAID remains elusive. However, neutrophils and macrophages are the main drivers of autoinflammation. In order to dissect the pathogenicity of disease we analyse the transcriptome of neutrophils and macrophages extracted from newly established APLAID mutant mice. Overall design: Comparative gene expression profiling analysis of macrophages and neutrophils samples from skin and lung of APLAID mutant and control mice.