scholarly journals Th2 cytokines impair innate immune responses to rhinovirus in respiratory epithelial cells

Allergy ◽  
2015 ◽  
Vol 70 (8) ◽  
pp. 910-920 ◽  
Author(s):  
M. Contoli ◽  
K. Ito ◽  
A. Padovani ◽  
D. Poletti ◽  
B. Marku ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Innate Immune ◽  
Th2 Cytokines ◽  
Innate Immune Responses ◽  
Respiratory Epithelial Cells ◽  
Respiratory Epithelial

scholarly journals Herpes Simplex Virus 1 Infection of Neuronal and Non-Neuronal Cells Elicits Specific Innate Immune Responses and Immune Evasion Mechanisms

2021 ◽  
Vol 12 ◽  
Author(s):  
Amanda L. Verzosa ◽  
Lea A. McGeever ◽  
Shun-Je Bhark ◽  
Tracie Delgado ◽  
Nicole Salazar ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Host Cell ◽  
Signaling Pathways ◽  
Sensory Neurons ◽  
Immune Evasion ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Hsv 1

Alphaherpesviruses (α-HV) are a large family of double-stranded DNA viruses which cause many human and animal diseases. There are three human α-HVs: Herpes Simplex Viruses (HSV-1 and HSV-2) and Varicella Zoster Virus (VZV). All α-HV have evolved multiple strategies to suppress or exploit host cell innate immune signaling pathways to aid in their infections. All α-HVs initially infect epithelial cells (primary site of infection), and later spread to infect innervating sensory neurons. As with all herpesviruses, α-HVs have both a lytic (productive) and latent (dormant) stage of infection. During the lytic stage, the virus rapidly replicates in epithelial cells before it is cleared by the immune system. In contrast, latent infection in host neurons is a life-long infection. Upon infection of mucosal epithelial cells, herpesviruses immediately employ a variety of cellular mechanisms to evade host detection during active replication. Next, infectious viral progeny bud from infected cells and fuse to neuronal axonal terminals. Here, the nucleocapsid is transported via sensory neuron axons to the ganglion cell body, where latency is established until viral reactivation. This review will primarily focus on how HSV-1 induces various innate immune responses, including host cell recognition of viral constituents by pattern-recognition receptors (PRRs), induction of IFN-mediated immune responses involving toll-like receptor (TLR) signaling pathways, and cyclic GMP‐AMP synthase stimulator of interferon genes (cGAS-STING). This review focuses on these pathways along with other mechanisms including autophagy and the complement system. We will summarize and discuss recent evidence which has revealed how HSV-1 is able to manipulate and evade host antiviral innate immune responses both in neuronal (sensory neurons of the trigeminal ganglia) and non-neuronal (epithelial) cells. Understanding the innate immune response mechanisms triggered by HSV-1 infection, and the mechanisms of innate immune evasion, will impact the development of future therapeutic treatments.

scholarly journals Glycosylation of Candida albicans Cell Wall Proteins Is Critical for Induction of Innate Immune Responses and Apoptosis of Epithelial Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50518 ◽  
Author(s):  
Jeanette Wagener ◽  
Günther Weindl ◽  
Piet W. J. de Groot ◽  
Albert D. de Boer ◽  
Susanne Kaesler ◽  
...  
Keyword(s):  
Cell Wall ◽  
Candida Albicans ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Innate Immune ◽  
Cell Wall Proteins ◽  
Innate Immune Responses
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