Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/35530
Title: The cell fate regulator NUPR1 is induced by Mycobacterium leprae via type I interferon in human leprosy
Authors: Andrade, Priscila R.
Mehta, Manali
Lu, Jing
Teles, Rosane M. B.
Montoya, Dennis
Scumpia, Phillip O.
Sarno, Euzenir Nunes
Ochoa, Maria Teresa
Ma, Feiyang
Pellegrini, Matteo
Modlin, Robert L.
Affilliation: University of California Los Angeles. David Geffen School of Medicine. Department of Dermatology. Los Angeles, CA, USA.
University of California Los Angeles. David Geffen School of Medicine. Department of Dermatology. Los Angeles, CA, USA
University of California Los Angeles. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.
University of California Los Angeles. David Geffen School of Medicine. Department of Dermatology. Los Angeles, CA, USA.
University of California Los Angeles. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.
University of California Los Angeles. David Geffen School of Medicine. Department of Dermatology. Los Angeles, CA, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.
University of Southern California School of Medicine. Department of Dermatology. Los Angeles, CA, USA.
University of California Los Angeles. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.
University of California Los Angeles. Department of Molecular, Cell, and Developmental Biology. Los Angeles, CA, USA.
University of California Los Angeles. David Geffen School of Medicine. Department of Dermatology. Los Angeles, CA, USA / University of California Los Angeles. Department of Microbiology, Immunology and Molecular Genetics. Los Angeles, CA, USA.
Abstract: The initial interaction between a microbial pathogen and the host immune response influences the outcome of the battle between the host and the foreign invader. Leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, provides a model to study relevant human immune responses. Previous studies have adopted a targeted approach to investigate host response to M. leprae infection, focusing on the induction of specific molecules and pathways. By measuring the host transcriptome triggered by M. leprae infection of human macrophages, we were able to detect a host gene signature 24-48 hours after infection characterized by specific innate immune pathways involving the cell fate mechanisms autophagy and apoptosis. The top upstream regulator in the M. leprae-induced gene signature was NUPR1, which is found in the M. leprae-induced cell fate pathways. The induction of NUPR1 by M. leprae was dependent on the production of the type I interferon (IFN), IFN-β. Furthermore, NUPR1 mRNA and protein were upregulated in the skin lesions from patients with the multibacillary form of leprosy. Together, these data indicate that M. leprae induces a cell fate program which includes NUPR1 as part of the host response in the progressive form of leprosy.
Keywords: Mycobacterium leprae
T cell
Regulator NUPR1
Type I Interferon
Human leprosy
keywords: Mycobacterium leprae
Regulador do destino celular
Interferon tipo I
Hanseníase humana
NUPR1
Issue Date: 2019
Publisher: Public Library of Science
Citation: ANDRADE, Priscila R. et al. The cell fate regulator NUPR1 is induced by Mycobacterium leprae via type I interferon in human leprosy. PLoS Neglected Tropical Diseases, v. 13, n. 7, p. 1-18, July 2019.
DOI: 10.1371/journal.pntd.0007589
ISSN: 1935-2727
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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