Toll-like receptor 8 (TLR8) polymorphisms are associated with non-progression of chronic hepatitis C in HIV/HCV coinfected patients

Fernández‐Rodríguez, Amanda; Berenguer, Juan; Jiménez‐Sousa, María A.; García–Álvarez, Mónica; Aldámiz‐Echevarría, Teresa; Pineda‐Tenor, Daniel; Díez, Cristina; Barrera, Jorge de la; Bellón, José M.; Briz, Verónica; Resino, Salvador

doi:10.1016/j.meegid.2015.10.006

Cited by 6 publications

(2 citation statements)

References 29 publications

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“…Further, HCV sensing by TLR7 occurs in both plasmacytoid dendritic cells (pDCs) and Kupffer cells, leading to production of IFN or activation of inflammasome (a multiprotein complex which plays a role in the innate immune response [41]. TLR7 and TLR8 share a high degree of structural similarity and variations in these genes, and impair immune responses during HCV infection [42,43]. Both activation and suppression of TLRs may be necessary to strengthen the anti-HCV immune response for limiting virus replication.…”

Section: Endogenous Interferon Productionmentioning

confidence: 99%

Strategies to Circumvent Host Innate Immune Response by Hepatitis C Virus

Patra

Ray

2019

Cells

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Innate immune responses generate interferons, proinflammatory cytokines, complement activation, and natural killer (NK) cell response. Ultimately, this leads to the induction of a robust virus-specific adaptive immunity. Although the host innate immune system senses and responds to eliminate virus infection, hepatitis C virus (HCV) evades immune attack and establishes persistent infection within the liver. Spontaneous clearance of HCV infection is associated with a prompt induction of innate immunity generated in an infected host. In this review, we have highlighted the current knowledge of our understanding of host–HCV interactions, especially for endogenous interferon production, proinflammatory response, NK cell response, and complement activation, which may impair the generation of a strong adaptive immune response for establishment of chronicity. The information may provide novel strategies in augmenting therapeutic intervention against HCV.

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Section: Endogenous Interferon Productionmentioning

confidence: 99%

Strategies to Circumvent Host Innate Immune Response by Hepatitis C Virus

Patra

Ray

2019

Cells

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“…A higher susceptibility and severity of infections caused by N. meningitidis are indeed related to alterations in the innate immune mechanisms rather than to mutations involving the acquired immune system [ 16 ]. Increasing evidence has showed that the presence of SNPs in Toll-like receptor ( TLR ) genes can represent a risk factor for IMD onset [ 2 ], as described also for other infectious diseases [ 17 , 18 , 19 , 20 ]. TLRs play a fundamental role in the recognition of pathogen associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), bacterial lipoproteins or unmethylated Cytosine-phosphate-Guanine (CpG) motifs, sensed by TLR4, TLR2 and TLR9, respectively [ 21 , 22 , 23 ].…”

Section: N Meningitidis Infection and Tlr Signmentioning

confidence: 99%

N. meningitidis and TLR Polymorphisms: A Fascinating Immunomodulatory Network

et al. 2016

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N. meningitidis infections represent a global health problem that can lead to the development of serious permanent sequelae. Although the use of antibiotics and prevention via vaccination have reduced the incidence of meningococcal disease, our understanding regarding N. meningitidis pathogenesis is still limited, especially of those mechanisms responsible for IMD and fulminant or deadly septic shock. These severe clinical presentations occur in a limited number of subjects, whereas about 10% of healthy individuals are estimated to carry the bacteria as a commensal. Since TLR activation is involved in the defense against N. meningitidis, several studies have highlighted the association between host TLR SNPs and a higher susceptibility and severity of N. meningitidis infections. Moreover, TLR SNPs induced variations in immunological responses and in their persistence upon vaccination against meningococcal disease. In the absence of mass vaccination programs, the early identification of risk factors for meningococcal disease would be recommended in order to start immunization strategies and antibiotic treatment in those subjects carrying the risk variants. In addition, it could allow us to identify individuals with a higher risk for severe disease and sequelae in order to develop a personalized healthcare of high-risk subjects based on their genomic profile. In this review, we have illustrated important preliminary correlations between TLR variants and meningococcal susceptibility/severity and with vaccine-induced immune responses.

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