About this Research Topic
Natural killer (NK) cells are cytotoxic lymphocytes which are potent to directly recognize and kill foreign cells, transformed or stressed self-cells during virus infection, malignancy, and physical or chemical trauma by mean of cytotoxic molecules (perforin and granzymes), cell surface expressed death ligands (TRAIL and FasL) or antibody-dependent cellular cytotoxicity. Activated NK cells also secrete various molecules such as IFN-γ, IL-10, TNF-α, GM-CSF or CCL5 to regulate or recruit other immune cells. Recent advances in immunology revealed various NK cell subsets with high diversity based on inhibitory-activating receptors, transcription factors and tissue distribution in mice and humans. Usually the peripheral blood of healthy individuals contains a dominating CD56Dim and a small proportion of CD56Bright subset which are equivalent to mouse mature (CD11b+CD27–) and immature (CD11b–CD27+) tissue resident NK cells respectively. The CD56Bright subset represents less differentiated tissue-resident NK cells and are efficient in cytokines production, whereas CD56Dim cells are mature and highly cytotoxic. Viral infections lead to the expansion of specific repertoires of NK cells, suggesting the involvement of distinctive NK cell subsets with high diversity.
The prime role of NK cells is to quickly eliminate infected cells to constrain the viral spread. However, NK cells can also inhibit or kill non-infected activated antiviral T cells and promote viral persistence. Whether these variable responses depend on different NK cell subsets is not known. NK cells during virus infection can change their phenotypic and functional behavior and convert into an existing or a new subset suggesting their plastic nature. In chronic HIV and HCV infection, an exhausted CD56– NK cell subset appears, which is associated with higher viral load. Memory-like NK cells with enhanced effector functions emerge in CMV infection of mouse and human, HIV infection, and in hepatitis A/B vaccinated people. Additionally, antiretroviral therapies are associated with enhanced CD56Bright NK subset and undetectable HIV load. This shift in the NK cell compartment is at the expense of other subsets that directs towards NK cell plasticity.
The NK plasticity decreases NK cell diversity due to expansion and persistence of a discrete NK cell subset. These changes in the NK cell compartment could be responsible for alteration in antiviral immune responses, viral load and disease pathogenicity for ongoing or subsequent same or different viral infections. Understanding the specific pathways influencing NK cell plasticity and diversity could provide new targets for therapeutic intervention to boost antiviral immunity.
In this collection we are interested to understand the mechanisms of NK cell plasticity and diversity, and its impact on antiviral immune responses in animal models or human settings. We welcome the submission of Original Research, Review, Mini Review and perspective articles to cover the following specific questions:
• Phenotypic and functional plasticity of NK cells and its influence on NK cell diversity in acute and chronic viral infections
• NK cell plasticity and diversity in antiviral therapies
• NK cell subset specific immune response in viral vaccination
• Regulators of NK cell plasticity and diversity
• Effect of NK cell plasticity and diversity on viral control
• Influence of NK cell diversification on subsequent viral infections, and its advantages and disadvantages
The prime role of NK cells is to quickly eliminate infected cells to constrain the viral spread. However, NK cells can also inhibit or kill non-infected activated antiviral T cells and promote viral persistence. Whether these variable responses depend on different NK cell subsets is not known. NK cells during virus infection can change their phenotypic and functional behavior and convert into an existing or a new subset suggesting their plastic nature. In chronic HIV and HCV infection, an exhausted CD56– NK cell subset appears, which is associated with higher viral load. Memory-like NK cells with enhanced effector functions emerge in CMV infection of mouse and human, HIV infection, and in hepatitis A/B vaccinated people. Additionally, antiretroviral therapies are associated with enhanced CD56Bright NK subset and undetectable HIV load. This shift in the NK cell compartment is at the expense of other subsets that directs towards NK cell plasticity.
The NK plasticity decreases NK cell diversity due to expansion and persistence of a discrete NK cell subset. These changes in the NK cell compartment could be responsible for alteration in antiviral immune responses, viral load and disease pathogenicity for ongoing or subsequent same or different viral infections. Understanding the specific pathways influencing NK cell plasticity and diversity could provide new targets for therapeutic intervention to boost antiviral immunity.
In this collection we are interested to understand the mechanisms of NK cell plasticity and diversity, and its impact on antiviral immune responses in animal models or human settings. We welcome the submission of Original Research, Review, Mini Review and perspective articles to cover the following specific questions:
• Phenotypic and functional plasticity of NK cells and its influence on NK cell diversity in acute and chronic viral infections
• NK cell plasticity and diversity in antiviral therapies
• NK cell subset specific immune response in viral vaccination
• Regulators of NK cell plasticity and diversity
• Effect of NK cell plasticity and diversity on viral control
• Influence of NK cell diversification on subsequent viral infections, and its advantages and disadvantages
Keywords: NK cells, antiviral immunity
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