Meta-Analysis and Bias

Fine, Bernard J.

doi:10.1126/science.250.4980.494-a

Cited by 89 publications

(102 citation statements)

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“…In peripheral blood, the virus is present in small resting memory B cells with latent gene expression limited to EBER, LMP2a, and perhaps EBNA1 [19]. It is well known that the interleukin 10 (IL-10) coding sequence is highly homologous to the EBV open reading frame BCRF1 [23]. BCRF1 protein, also termed viral IL-10 (vIL-10), inhibits the synthesis of T-helper 1 cytokines [24] and cytotoxic T lymphocytes (CTL) activity [25].…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Epstein–Barr virus in tonsils and adenoids of United Arab Emirates nationals

Al-Salam

Dhaheri

Awwad

et al. 2011

International Journal of Pediatric Otorhinolaryngology

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Section: Discussionmentioning

confidence: 99%

Prevalence of Epstein–Barr virus in tonsils and adenoids of United Arab Emirates nationals

Al-Salam

Dhaheri

Awwad

et al. 2011

International Journal of Pediatric Otorhinolaryngology

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“…Among these mechanisms, large DNA viruses encode for protein homologs of cytokines and chemokines or express viral factors that alter host cytokine production [179,180]. Members of the representative latency-inducing Herpesviridae family, such as human cytomegalovirus (HCMV) [181], Epstein-Barr virus (EBV) [182], ovine herpesvirus 2 [183], and equine herpesvirus 2 [184], encode for IL-10 homologs. Among the best-characterized IL-10 homologs are the cytomegalovirusencoded IL-10, termed cmvIL-10, and the latency-associated cmvIL-10, termed LAcmvIL-10 [181,185] (Figure 1).…”

Section: Viral Il-10 Homologs In Chronic and Latent Infectionsmentioning

confidence: 99%

IL-10: A Multifunctional Cytokine in Viral Infections

Rojas

Avia

Martı́n

et al. 2017

Journal of Immunology Research

299

268

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The anti-inflammatory master regulator IL-10 is critical to protect the host from tissue damage during acute phases of immune responses. This regulatory mechanism, central to T cell homeostasis, can be hijacked by viruses to evade immunity. IL-10 can be produced by virtually all immune cells, and it can also modulate the function of these cells. Understanding the effects of this multifunctional cytokine is therefore a complex task. In the present review we discuss the factors driving IL-10 production and the cellular sources of the cytokine during antiviral immune responses. We particularly focus on the IL-10 regulatory mechanisms that impact antiviral immune responses and how viruses can use this central regulatory pathway to evade immunity and establish chronic/latent infections.

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“…Among these cytokines was mouse cytokine synthesis inhibitory factor produced by Th2 cells, later renamed interleukin 10. 14,15 Interleukin 10 is a type 2 cytokine and the fi rst identifi ed member of a family of cytokines that include interleukins 19, 20, 22, 24, 26, 28, and 29. 16 All these cytokines have similar genomic organisation, bind to receptors with similar structures and, in some cases, shared components, and all activate Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling pathways.…”

Section: Protozoan Parasitism Of Macrophagesmentioning

confidence: 99%

Intrinsic antibody-dependent enhancement of microbial infection in macrophages: disease regulation by immune complexes

Halstead

Mahalingam

Marovich

et al. 2010

The Lancet Infectious Diseases

347

308

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A wide range of microorganisms can replicate in macrophages, and cell entry of these pathogens via non-neutralising IgG antibody complexes can result in increased intracellular infection through idiosyncratic Fcγ-receptor signalling. The activation of Fcγ receptors usually leads to phagocytosis. Paradoxically, the ligation of monocyte or macrophage Fcγ receptors by IgG immune complexes, rather than aiding host defences, can suppress innate immunity, increase production of interleukin 10, and bias T-helper-1 (Th1) responses to Th2 responses, leading to increased infectious output by infected cells. This intrinsic antibody-dependent enhancement (ADE) of infection modulates the severity of diseases as disparate as dengue haemorrhagic fever and leishmaniasis. Intrinsic ADE is distinct from extrinsic ADE, whereby complexes of infectious agents with non-neutralising antibodies lead to an increased number of infected cells. Intrinsic ADE might be involved in many protozoan, bacterial, and viral infections. We review insights into intracellular mechanisms and implications of enhanced pathogenesis after ligation of macrophage Fcγ receptors by infectious immune complexes.

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Meta-Analysis and Bias

Cited by 89 publications

References 1 publication

Prevalence of Epstein–Barr virus in tonsils and adenoids of United Arab Emirates nationals

Prevalence of Epstein–Barr virus in tonsils and adenoids of United Arab Emirates nationals

IL-10: A Multifunctional Cytokine in Viral Infections

Intrinsic antibody-dependent enhancement of microbial infection in macrophages: disease regulation by immune complexes

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