scholarly journals Bystanders or real players: virtual memory T cells keep chronic infections in check

2020 ◽  
Vol 17 (8) ◽  
pp. 797-798
Author(s):  
Kylie M. Quinn ◽  
Tabinda Hussain
2021 ◽  
Author(s):  
Ruth K. Nyakundi ◽  
Jann Hau ◽  
Paul Ogongo ◽  
Onkoba Nyamongo ◽  
Maamum Jeneby ◽  
...  

Background. Naturally acquired immunity to malaria develops over several years and can be compromised by concomitant infections. This study explored the influence of chronic schistosomiasis on clinical outcome and immunity to repeated malaria infection. Methods. Two groups of baboons (n=8 each), were infected with Schistosoma mansoni cercariae to establish chronic infections. One of the two groups was treated with Praziquantel to eliminate schistosome infection. The two groups plus a new malaria control group (n=8), were inoculated three times with Plasmodium knowlesi parasites at one-month intervals. Clinical data, IgG, IgG1, memory T-cells and monocyte levels were recorded. Results. We observed after three P. knowlesi infections; i) reduced clinical symptoms in all groups with each subsequent infection, ii) increase IgG and IgG1in the malaria control (Pk-only) group iii) increased IgG and IgG1, CD14 + and CD14 - CD16 + in the Schistosoma treated (Schisto/PZQ+Pk) group and iv) significantly lower IgG and IgG1 levels compared to Pk-only, reduced CD4 + CD45RO + and increased CD14 - CD16 + cells in the co-infected (Schisto+Pk) group. Conclusion. Chronic S. mansoni does not compromise establishment of clinical immunity after multiple malaria infections with non-classical monocytes seeming to play a role. Failure to develop robust antibody and memory T-cells may have a long-term impact on acquired immunity to malaria infection.


2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Jason T. White ◽  
Eric W. Cross ◽  
Matthew A. Burchill ◽  
Thomas Danhorn ◽  
Martin D. McCarter ◽  
...  

2019 ◽  
Vol 116 (20) ◽  
pp. 9969-9978 ◽  
Author(s):  
Andreia S. Da Costa ◽  
Jessica B. Graham ◽  
Jessica L. Swarts ◽  
Jennifer M. Lund

Immunological memory exists so that following infection an expanded population of pathogen-specific lymphocytes can rapidly and efficiently control infection in the case of reexposure. However, in the case of CD8+ T lymphocytes, a population of unconventional CD44+CD122+ virtual memory T cells (TVM) has been described that possesses many, though not all, features of “true memory” T cells, without the requirement of first encountering cognate antigen. Here, we demonstrate a role for regulatory T cell-mediated restraint of TVM at least in part through limiting IL-15 trans-presentation by CD11b+ dendritic cells. Further, we show that keeping TVM in check ensures development of functional, antigen-specific “true” memory phenotype CD8+ T cells that can assist in pathogen control upon reexposure.


2020 ◽  
Vol 21 (5) ◽  
pp. 499-500 ◽  
Author(s):  
Mark A. Daniels ◽  
Emma Teixeiro

2015 ◽  
Vol 45 (7) ◽  
pp. 1916-1920 ◽  
Author(s):  
Luc Van Kaer

Author(s):  
Eliza Mari Kwesi-Maliepaard ◽  
Heinz Jacobs ◽  
Fred van Leeuwen

AbstractConventional CD8+ memory T cells develop upon stimulation with foreign antigen and provide increased protection upon re-challenge. Over the past two decades, new subsets of CD8+ T cells have been identified that acquire memory features independently of antigen exposure. These antigen-inexperienced memory T cells (TAIM) are described under several names including innate memory, virtual memory, and memory phenotype. TAIM cells exhibit characteristics of conventional or true memory cells, including antigen-specific responses. In addition, they show responsiveness to innate stimuli and have been suggested to provide additional levels of protection toward infections and cancer. Here, we discuss the current understanding of TAIM cells, focusing on extrinsic and intrinsic molecular conditions that favor their development, their molecular definitions and immunological properties, as well as their transcriptional and epigenetic regulation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Maike Hofmann ◽  
Camilla Jandus ◽  
Lian Ni Lee ◽  
Daniel T. Utzschneider

2017 ◽  
Author(s):  
Ales Drobek ◽  
Alena Moudra ◽  
Daniel Mueller ◽  
Martina Huranova ◽  
Veronika Horkova ◽  
...  

AbstractVirtual memory T cells are foreign antigen-inexperienced T cells that have acquired memory-like phenotype and constitute for 10-20% of all peripheral CD8+ T cells in mice. Their origin, biological roles, and relationship to naïve and foreign antigen-experienced memory T cells are incompletely understood. By analyzing TCR repertoires and using retrogenic monoclonal T-cell populations, we show that virtual memory T cells originate exclusively from strongly self-reactive T cells. Moreover, we show that the stoichiometry of the CD8 interaction with Lck regulates the size of the virtual memory T-cell compartment via modulating the self-reactivity of individual T-cell clones. We propose a so far unappreciated peripheral T-cell fate decision checkpoint that eventually leads to the differentiation of highly self-reactive T cells into virtual memory T cells. This underlines the importance of the variable level of self-reactivity in polyclonal T cells for the generation of functional T-cell diversity. Although virtual memory T cells descend from the highly self-reactive clones and acquire a partial memory program, they do not show higher capacity to induce autoimmune diabetes than naïve T cells. Thus, virtual memory T cells are not generally more responsive than naïve T cells, because their activity highly depends on the immunological context.SummaryWe conclude that virtual memory T cells are formed from self-reactive CD8+ T cells in a process regulated by CD8-Lck stoichiometry. Despite their self-reactivity and partial memory differentiation program, virtual memory T cells did not show a strong autoimmune potential.


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