Shigella impairs human T lymphocyte responsiveness by hijacking actin cytoskeleton dynamics and T cell receptor vesicular trafficking.
Actin Cytoskeleton
/ metabolism
Actins
Adaptive Immunity
Cell Line
Dysentery, Bacillary
/ immunology
Golgi Apparatus
Humans
Immunological Synapses
Protein Transport
/ physiology
Receptors, Antigen, T-Cell
/ metabolism
Shigella
/ genetics
T-Lymphocytes
/ immunology
Type III Secretion Systems
/ metabolism
Shigella
Golgi
Rab proteins
T cell activation
T3SS effectors
TCR
actin
cell polarisation
immunological synapse
vesicular trafficking
Journal
Cellular microbiology
ISSN: 1462-5822
Titre abrégé: Cell Microbiol
Pays: India
ID NLM: 100883691
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
07
08
2019
revised:
18
12
2019
accepted:
18
12
2019
pubmed:
21
1
2020
medline:
3
6
2021
entrez:
21
1
2020
Statut:
ppublish
Résumé
Strategies employed by pathogenic enteric bacteria, such as Shigella, to subvert the host adaptive immunity are not well defined. Impairment of T lymphocyte chemotaxis by blockage of polarised edge formation has been reported upon Shigella infection. However, the functional impact of Shigella on T lymphocytes remains to be determined. Here, we show that Shigella modulates CD4+ T cell F-actin dynamics and increases cell cortical stiffness. The scanning ability of T lymphocytes when encountering antigen-presenting cells (APC) is subsequently impaired resulting in decreased cell-cell contacts (or conjugates) between the two cell types, as compared with non-infected T cells. In addition, the few conjugates established between the invaded T cells and APCs display no polarised delivery and accumulation of the T cell receptor to the contact zone characterising canonical immunological synapses. This is most likely due to the targeting of intracellular vesicular trafficking by the bacterial type III secretion system (T3SS) effectors IpaJ and VirA. The collective impact of these cellular reshapings by Shigella eventually results in T cell activation dampening. Altogether, these results highlight the combined action of T3SS effectors leading to T cell defects upon Shigella infection.
Identifiants
pubmed: 31957253
doi: 10.1111/cmi.13166
pmc: PMC7187243
doi:
Substances chimiques
Actins
0
Receptors, Antigen, T-Cell
0
Type III Secretion Systems
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13166Informations de copyright
© 2020 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd.
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