scholarly journals RIPK3 and Caspase-1/11 Are Necessary for Optimal Antigen-Specific CD8 T Cell Response Elicited by Genetically Modified Listeria monocytogenes

2020 ◽  
Vol 11 ◽  
Author(s):  
Aamir Rana ◽  
Felipe Campos de Almeida ◽  
Henry A. Paico Montero ◽  
Maryanne M. Gonzales Carazas ◽  
Karina R. Bortoluci ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
T Cell ◽  
Cell Response ◽  
Genetically Modified ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Caspase 1

scholarly journals Listeria Monocytogenes: A Model Pathogen Continues to Refine Our Knowledge of the CD8 T Cell Response

Pathogens ◽  
2018 ◽  
Vol 7 (2) ◽  
pp. 55 ◽  
Author(s):  
Zhijuan Qiu ◽  
Camille Khairallah ◽  
Brian Sheridan
Keyword(s):  
Listeria Monocytogenes ◽  
T Cell ◽  
Cell Response ◽  
Protective Immunity ◽  
T Cell Responses ◽  
Cd8 T Cell ◽  
Oral Infection ◽  
T Cell Response ◽  
Infection Model ◽  
Cell Responses

Listeria monocytogenes (Lm) infection induces robust CD8 T cell responses, which play a critical role in resolving Lm during primary infection and provide protective immunity to re-infections. Comprehensive studies have been conducted to delineate the CD8 T cell response after Lm infection. In this review, the generation of the CD8 T cell response to Lm infection will be discussed. The role of dendritic cell subsets in acquiring and presenting Lm antigens to CD8 T cells and the events that occur during T cell priming and activation will be addressed. CD8 T cell expansion, differentiation and contraction as well as the signals that regulate these processes during Lm infection will be explored. Finally, the formation of memory CD8 T cell subsets in the circulation and in the intestine will be analyzed. Recently, the study of CD8 T cell responses to Lm infection has begun to shift focus from the intravenous infection model to a natural oral infection model as the humanized mouse and murinized Lm have become readily available. Recent findings in the generation of CD8 T cell responses to oral infection using murinized Lm will be explored throughout the review. Finally, CD8 T cell-mediated protective immunity against Lm infection and the use of Lm as a vaccine vector for cancer immunotherapy will be highlighted. Overall, this review will provide detailed knowledge on the biology of CD8 T cell responses after Lm infection that may shed light on improving rational vaccine design.

scholarly journals The Onset of CD8+-T-Cell Contraction Is Influenced by the Peak of Listeria monocytogenes Infection and Antigen Display

2006 ◽  
Vol 74 (3) ◽  
pp. 1528-1536 ◽  
Author(s):  
Brandon B. Porter ◽  
John T. Harty
Keyword(s):  
Listeria Monocytogenes ◽  
T Cell ◽  
Cell Response ◽  
Direct Relationship ◽  
Lethal Dose ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Cell Responses ◽  
Listeria Monocytogenes Infection ◽  
Precise Time

ABSTRACT The CD8+-T-cell response to infection with Listeria monocytogenes consists of expansion, contraction, and memory phases. The transition between expansion and contraction is reported to occur on different days postinfection with virulent (8 to 9 days) and attenuated (ΔactA) (7 days) L. monocytogenes strains. We hypothesized that differences in the infectious courses, and therefore antigen (Ag) display, determine the precise time of the expansion/contraction transition in response to these infections. To test this, we infected BALB/c mice with 0.1 50% lethal dose of ΔactA or virulent L. monocytogenes and measured bacterial numbers, Ag display, and Ag-specific CD8+-T-cell responses on various days after infection. We found that bacterial numbers and Ag display peaked between 12 and 36 h and between 36 and 60 h after infection with ΔactA and virulent L. monocytogenes strains, respectively. Infection with ΔactA L. monocytogenes resulted in a sharp peak in the Ag-specific CD8+-T-cell response on day 7, while infection with virulent L. monocytogenes yielded a prolonged peak with equivalent numbers of Ag-specific CD8+ T cells on days 6, 7, and 8 after infection. Truncating virulent infection with antibiotics on day 1 or 2 after infection resulted in a shift in the expansion/contraction transition from day 8 to day 7 after infection. However, antibiotic treatment beginning on day 3, after the peak of virulent L. monocytogenes infection and Ag display, had no effect upon the magnitude or timing of the CD8+-T-cell response. These results demonstrate a direct relationship between the course of infection and Ag display and that the timing of these events is important in shaping the T-cell response to infection.

scholarly journals A Potential New Pathway for PD-L1 Costimulation of the CD8-T Cell Response to Listeria monocytogenes Infection

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56539 ◽  
Author(s):  
Daqi Xu ◽  
Han-Hsuan Fu ◽  
Joshua J. Obar ◽  
Jang-June Park ◽  
Koji Tamada ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
T Cell ◽  
Cell Response ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Listeria Monocytogenes Infection

scholarly journals Enumeration of Cytotoxic CD8 T Cells Ex Vivo during the Response to Listeria monocytogenes Infection

2008 ◽  
Vol 76 (10) ◽  
pp. 4609-4614 ◽  
Author(s):  
Dietmar M. W. Zaiss ◽  
Alice J. A. M. Sijts ◽  
Tim R. Mosmann
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
T Cell ◽  
Cytotoxic Activity ◽  
Cd8 T Cells ◽  
Cell Response ◽  
Ex Vivo ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Ifn Γ

ABSTRACT Cytotoxicity is a key effector function of CD8 T cells. However, what proportion of antigen-specific CD8 T cells in vivo exert cytotoxic activity during a functional CD8 T-cell response to infection still remains unknown. We used the Lysispot assay to directly enumerate cytotoxic CD8 T cells from the spleen ex vivo during the immune response to infection with the intracellular bacterium Listeria monocytogenes. We demonstrate that not all antigen-responsive gamma interferon (IFN-γ)-secreting T cells display cytotoxic activity. Most CD8 T cells detected at early time points of the response were cytotoxic. This percentage continuously declined during both the expansion and contraction phases to about 50% at the peak and to <10% of IFN-γ-producing cells in the memory phase. As described for clonal expansion, this elaboration of a program of differentiation after an initial stimulus was not affected by antigen or CD4 help but, like proliferation, could be influenced by later reinfection. These data indicate that cytotoxic effector function during the response to infection is regulated independently from IFN-γ secretion or expansion or contraction of the overall CD8 T-cell response.

scholarly journals An epidemic Zika virus isolate suppresses antiviral immunity by disrupting antigen presentation pathways

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ryan D. Pardy ◽  
Stefanie F. Valbon ◽  
Brendan Cordeiro ◽  
Connie M. Krawczyk ◽  
Martin J. Richer
Keyword(s):  
T Cell ◽  
Zika Virus ◽  
Cell Response ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Cross Presentation ◽  
Cell Immunity ◽  
Asian Lineage ◽  
Insight Into ◽  
Host Tissues

AbstractZika virus (ZIKV) has emerged as an important global health threat, with the recently acquired capacity to cause severe neurological symptoms and to persist within host tissues. We previously demonstrated that an early Asian lineage ZIKV isolate induces a highly activated CD8 T cell response specific for an immunodominant epitope in the ZIKV envelope protein in wild-type mice. Here we show that a contemporary ZIKV isolate from the Brazilian outbreak severely limits CD8 T cell immunity in mice and blocks generation of the immunodominant CD8 T cell response. This is associated with a more sustained infection that is cleared between 7- and 14-days post-infection. Mechanistically, we demonstrate that infection with the Brazilian ZIKV isolate reduces the cross-presentation capacity of dendritic cells and fails to fully activate the immunoproteasome. Thus, our study provides an isolate-specific mechanism of host immune evasion by one Brazilian ZIKV isolate, which differs from the early Asian lineage isolate and provides potential insight into viral persistence associated with recent ZIKV outbreaks.

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