NLRP6 Deficiency in CD4 T Cells Decreases T Cell Survival Associated with Increased Cell Death.

Details

Serval ID
serval:BIB_FB1F4EA9ABB0
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
NLRP6 Deficiency in CD4 T Cells Decreases T Cell Survival Associated with Increased Cell Death.
Journal
Journal of immunology
Author(s)
Radulovic K., Ayata C.K., Mak'Anyengo R., Lechner K., Wuggenig P., Kaya B., Hruz P., Gomez de Agüero M., Broz P., Weigmann B., Niess J.H.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Publication state
Published
Issued date
15/07/2019
Peer-reviewed
Oui
Volume
203
Number
2
Pages
544-556
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The nucleotide-binding oligomerization domain (NOD)-like receptors belong to the family of pattern recognition receptors (PRRs). NOD-like receptors play a role in regulation of innate immune response by recognition of both pathogen-associated molecular patterns that are engulfed during phagocytic process and danger-associated molecular patterns that are mainly byproducts of cell stress mediated response. NOD-like family pyrin domain containing 6 (NLRP6) is one of the 14 pyrin domain-containing receptors. NLRP6 is highly expressed by epithelial and goblet cells to regulate epithelial renewal and mucus production in mice and humans, but its function in T cells is rather unknown. Increased caspase-1 activation and cell death were observed in mouse Nlrp6-deficient T cells following adoptive transfer into Rag2-deficient mice, indicating that Nlrp6 deficiency in CD4 <sup>+</sup> T cells led to decreased survival.
Keywords
Adoptive Transfer/methods, Animals, CD4-Positive T-Lymphocytes/immunology, Cell Death, Cell Survival/immunology, Epithelial Cells/immunology, Goblet Cells/immunology, Immunity, Innate/immunology, Mice, Mice, Inbred C57BL, Receptors, Cell Surface/deficiency, Receptors, Cell Surface/immunology
Pubmed
Web of science
Create date
17/06/2019 18:39
Last modification date
18/02/2020 7:20
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