Type I Interferon Responses by HIV-1 Infection: Association with Disease Progression and Control

Soper, Andrew; Kimura, Izumi; Nagaoka, Sumiharu; Konno, Yoriyuki; Yamamoto, Keisuke; Koyanagi, Yoshio; Sato, Kei

doi:10.3389/fimmu.2017.01823

Cited by 70 publications

(63 citation statements)

References 128 publications

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“…We also found that SLAMF7 signaling in human monocytes inhibits the production of various alpha chemokines, but not host restriction factors that are critical for combatting HIV-1 infection at the cellular level. These results have major implications, not only in HIV-associated pathogenesis, but also for other type I interferonopathies [102]. These discoveries suggest that SLAMF7 activation on monocytes of HIV infected individuals has the potential to prevent HIV infection of monocytes as well as pathogenic type I interferon signaling, all while sparing critical HIV host-restriction factors.…”

Section: Potential For Targeting Slam Family Of Receptors In Hiv Andmentioning

confidence: 87%

SLAM Family Receptor Signaling in Viral Infections: HIV and Beyond

2019

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The signaling lymphocytic activation molecule (SLAM) family of receptors are expressed on the majority of immune cells. These receptors often serve as self-ligands, and play important roles in cellular communication and adhesion, thus modulating immune responses. SLAM family receptor signaling is differentially regulated in various immune cell types, with responses generally being determined by the presence or absence of two SLAM family adaptor proteins—Ewing’s sarcoma-associated transcript 2 (EAT-2) and SLAM-associated adaptor protein (SAP). In addition to serving as direct regulators of the immune system, certain SLAM family members have also been identified as direct targets for specific microbes and viruses. Here, we will discuss the known roles for these receptors in the setting of viral infection, with special emphasis placed on HIV infection. Because HIV causes such complex dysregulation of the immune system, studies of the roles for SLAM family receptors in this context are particularly exciting.

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Section: Potential For Targeting Slam Family Of Receptors In Hiv Andmentioning

confidence: 87%

SLAM Family Receptor Signaling in Viral Infections: HIV and Beyond

2019

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“…IFNα has been shown to inhibit both HIV-1 replication and IL-1β expression (15,56). Thus, we next sought to probe the expression of IL-1β and miR-146a expression in IFNα treated HIV-1 infected CD4 + T-cells.…”

Section: Ifnα Treatment Inhibits Hiv-1 Replication and Disrupts Il-1βmentioning

confidence: 99%

Methamphetamine Enhances HIV-1 Replication in CD4+ T-Cells via a Novel IL-1β Auto-Regulatory Loop

Lawson

Groopman

2020

Front. Immunol.

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Methamphetamine (Meth) abuse is a worldwide public health problem and contributes to HIV-1 pathobiology and poor adherence to anti-retroviral therapies. Specifically, Meth is posited to alter molecular mechanisms to provide a more conducive environment for HIV-1 replication and spread. Enhanced expression of inflammatory cytokines, such as Interleukin-1β (IL-1β), has been shown to be important for HIV-1 pathobiology. In addition, microRNAs (miRNAs) play integral roles in fine-tuning the innate immune response. Notably, the effects of Meth abuse on miRNA expression are largely unknown. We studied the effects of Meth on IL-1β and miR-146a, a well-characterized member of the innate immune signaling network. We found that Meth induces miR-146a and triggers an IL-1β auto-regulatory loop to modulate innate immune signaling in CD4 + T-cells. We also found that Meth enhances HIV-1 replication via IL-1 signaling. Our results indicate that Meth activates an IL-1β feedback loop to alter innate immune pathways and favor HIV-1 replication. These observations offer a framework for designing targeted therapies in HIV-infected, Meth using hosts.

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“…Type I interferons (IFN) are a major line of host defence against viruses and other microorganisms 1. However, it is now clear that type I IFNs can also drive context-specific responses to infection, which may be either beneficial or detrimental to the host 2–4. Furthermore, dysregulation of the type I IFN system can elicit autoimmune diseases, perhaps best exemplified by interferonopathies and SLE 5.…”

Section: Introductionmentioning

confidence: 99%

Type I interferons in host defence and inflammatory diseases

Crow

Rönnblom

2019

Lupus Sci Med

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Type I interferons (IFN) can have dual and opposing roles in immunity, with effects that are beneficial or detrimental to the individual depending on whether IFN pathway activation is transient or sustained. Determinants of IFN production and its functional consequences include the nature of the microbial or nucleic acid stimulus, the type of nucleic acid sensor involved in inducing IFN, the predominant subtype of type I IFN produced and the immune ecology of the tissue at the time of IFN expression. When dysregulated, the type I IFN system drives many autoimmune and non-autoimmune inflammatory diseases, including SLE and the tissue inflammation associated with chronic infection. The type I IFN system may also contribute to outcomes for patients affected by solid cancers or myocardial infarction. Significantly more research is needed to discern the mechanisms of induction and response to type I IFNs across these diseases, and patient endophenotyping may help determine whether the cytokine is acting as ‘friend’ or ‘foe’, within a particular patient, and at the time of treatment. This review summarises key concepts and discussions from the second International Summit on Interferons in Inflammatory Diseases, during which expert clinicians and scientists evaluated the evidence for the role of type I IFNs in autoimmune and other inflammatory diseases.

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Type I Interferon Responses by HIV-1 Infection: Association with Disease Progression and Control

Cited by 70 publications

References 128 publications

SLAM Family Receptor Signaling in Viral Infections: HIV and Beyond

SLAM Family Receptor Signaling in Viral Infections: HIV and Beyond

Methamphetamine Enhances HIV-1 Replication in CD4+ T-Cells via a Novel IL-1β Auto-Regulatory Loop

Type I interferons in host defence and inflammatory diseases

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