Disruption of an antimycobacterial circuit between dendritic and helper T cells in human SPPL2a deficiency

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art_KONG_Disruption_of_an_antimycobacterial_circuit_between_dendritic_and_2018.PDF (2.88 MB)
Citações na Scopus
91
Tipo de produção
article
Data de publicação
2018
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
NATURE PUBLISHING GROUP
Autores
KONG, Xiao-Fei
MARTINEZ-BARRICARTE, Ruben
KENNEDY, James
MELE, Federico
LAZAROV, Tomi
DEENICK, Elissa K.
MA, Cindy S.
BRETON, Gaelle
LUCERO, Kimberly B.
LANGLAIS, David
Citação
NATURE IMMUNOLOGY, v.19, n.9, p.973-985, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Human inborn errors of IFN-gamma immunity underlie mycobacterial diseases. We describe patients with Mycobacterium bovis (BCG) disease who are homozygous for loss-of-function mutations of SPPL2A. This gene encodes a transmembrane protease that degrades the N-terminal fragment (NTF) of CD74 (HLA invariant chain) in antigen-presenting cells. The CD74 NTF therefore accumulates in the HLA class II+ myeloid and lymphoid cells of SPPL2a-deficient patients. This toxic fragment selectively depletes IL-12-and IL-23-producing CD1c(+) conventional dendritic cells (cDC2s) and their circulating progenitors. Moreover, SPPL2a-deficient memory T(H)1(star) cells selectively fail to produce IFN-gamma when stimulated with mycobacterial antigens in vitro. Finally, Sppl2a(-/-) mice lack cDC2s, have CD4(+) T cells that produce small amounts of IFN-gamma after BCG infection, and are highly susceptible to infection with BCG or Mycobacterium tuberculosis. These findings suggest that inherited SPPL2a deficiency in humans underlies mycobacterial disease by decreasing the numbers of cDC2s and impairing IFN-gamma production by mycobacterium-specific memory T(H)1(star) cells.
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https://observatorio.fm.usp.br/handle/OPI/28336
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Coleções
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/56
Artigos e Materiais de Revistas Científicas - ODS/03