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© 2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

A mobile element designated ICE(r2) (NJ56_RS12425-NJ56_RS12600) in the SC09 strain is integrated between an intact or partial tRNA-Asn copy. [...]a class of bacterial proteins homologous to the Toll/IL-1 receptor (TIR) domain was identified; these proteins were encoded by ICE(r2) and acted as accessory genes. [...]is has been shown that a TIR-containing protein in the SC09 strain, STIR-2, targets TLR signaling to facilitate escape from the host innate immune response and enhance virulence. TIR domain interactions play a pivotal role in mediating innate immunity and identifying pathogens [28]. [...]it is reasonable to hypothesize that TIR domain-containing proteins (Tcps) from Y. ruckeri SC09 disrupt the TLR signal transduction system in host cells to facilitate escape from the host innate immune and enhance bacterial survival. 2.2. Bacterial adhesion (Figure 3A), invasion (Figure 3B), and the invasion ratio (number of intracellular bacteria/number of adherent bacteria) (Figure 3C) were not significantly different between the wild-type SC09 and SC09Δstir-2 mutant. [...]the stir-2 gene did not appear to enhance the ability of Y. ruckeri SC09 to adhere and invade rainbow trout macrophages.

Details

Title
A Yersinia ruckeri TIR Domain-Containing Protein (STIR-2) Mediates Immune Evasion by Targeting the MyD88 Adaptor
Author
Liu, Tao; Wen-Yan, Wei; Kai-Yu, Wang; Er-Long, Wang; Yang, Qian
Publication year
2019
Publication date
2019
Publisher
MDPI AG
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2333824602
Copyright
© 2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.