Armc5 deletion causes developmental defects and compromises T-cell immune responses

Yan Hu, Linjiang Lao, Jianning Mao, Wei Jin, Hongyu Luo, Tania Charpentier, Shijie Qi, Junzheng Peng, Bing Hu, Mieczyslaw Martin Marcinkiewicz, Alain Lamarre and Jiangping Wu ()
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Yan Hu: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Linjiang Lao: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Jianning Mao: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Wei Jin: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Hongyu Luo: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Tania Charpentier: Institut national de la recherche scientifique—Institut Armand-Frappier (INRS-IAF)
Shijie Qi: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Junzheng Peng: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)
Bing Hu: Anatomic Pathology, AmeriPath Central Florida
Mieczyslaw Martin Marcinkiewicz: Cytochem Inc.
Alain Lamarre: Institut national de la recherche scientifique—Institut Armand-Frappier (INRS-IAF)
Jiangping Wu: Centre de recherche (CR), Centre hospitalier de l’Université de Montréal (CHUM)

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Armadillo repeat containing 5 (ARMC5) is a cytosolic protein with no enzymatic activities. Little is known about its function and mechanisms of action, except that gene mutations are associated with risks of primary macronodular adrenal gland hyperplasia. Here we map Armc5 expression by in situ hybridization, and generate Armc5 knockout mice, which are small in body size. Armc5 knockout mice have compromised T-cell proliferation and differentiation into Th1 and Th17 cells, increased T-cell apoptosis, reduced severity of experimental autoimmune encephalitis, and defective immune responses to lymphocytic choriomeningitis virus infection. These mice also develop adrenal gland hyperplasia in old age. Yeast 2-hybrid assays identify 16 ARMC5-binding partners. Together these data indicate that ARMC5 is crucial in fetal development, T-cell function and adrenal gland growth homeostasis, and that the functions of ARMC5 probably depend on interaction with multiple signalling pathways.

Date: 2017
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DOI: 10.1038/ncomms13834

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