scholarly journals Regulation of the type I interferon genes and interferon-inducible genes. The relationship with the viral reproduction under HIV-infection

2001 ◽  
Vol 17 (5) ◽  
pp. 347-355
Author(s):  
A. V. Karpov
Keyword(s):  
Hiv Infection ◽  
Type I Interferon ◽  
Type I ◽  
Inducible Genes ◽  
The Relationship ◽  
Viral Reproduction

scholarly journals The Abstruse Side of Type I Interferon Immunotherapy for COVID-19 Cases with Comorbidities

2021 ◽  
Vol 1 (1) ◽  
pp. 49-59
Author(s):  
Selvakumar Subbian
Keyword(s):  
Infectious Diseases ◽  
Disease Severity ◽  
Type I Interferon ◽  
Host Factors ◽  
Type I ◽  
The Novel ◽  
Inflammatory Drugs ◽  
Precautionary Measures ◽  
Inducible Genes

The Coronavirus Disease-2019 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has claimed 1.2 million people globally since December 2019. Although the host factors underpinning COVID-19 pathology are not fully understood, type I interferon (IFN-I) response is considered crucial for SARS-CoV-2 pathogenesis. Perturbations in IFN-I signaling and associated interferon-inducible genes (ISG) are among the primary disease severity indicators in COVID-19. Consequently, IFN-I therapy, either alone or in- combination with existing antiviral or anti-inflammatory drugs, is tested in many ongoing clinical trials to reduce COVID-19 mortality. Since signaling by the IFN-I family of molecules regulates host immune response to other infectious and non-infectious diseases, any imbalance in this family of cytokines would impact the clinical outcome of COVID-19, as well as other co-existing diseases. Therefore, it is imperative to evaluate the beneficial-versus-detrimental effects of IFN-I immunotherapy for COVID-19 patients with divergent disease severity and other co-existing conditions. This review article summarizes the role of IFN-I signaling in infectious and non-infectious diseases of humans. It highlights the precautionary measures to be considered before administering IFN-I to COVID-19 patients having other co-existing disorders. Finally, suggestions are proposed to improve IFN-I immunotherapy to COVID-19.

scholarly journals B7–H3 regulates osteoclast differentiation via type I interferon-dependent IDO induction

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Younseo Oh ◽  
Robin Park ◽  
So Yeon Kim ◽  
Sung-ho Park ◽  
Sungsin Jo ◽  
...  
Keyword(s):  
Immune Checkpoint ◽  
Osteoblast Differentiation ◽  
Type I Interferon ◽  
Osteoclast Differentiation ◽  
Regulatory Function ◽  
Type I ◽  
Type I Ifn ◽  
B7 Family ◽  
Human Osteoclast ◽  
Inducible Genes

AbstractWhile their function, as immune checkpoint molecules, is well known, B7-family proteins also function as regulatory molecules in bone remodeling. B7–H3 is a receptor ligand of the B7 family that functions primarily as a negative immune checkpoint. While the regulatory function of B7–H3 in osteoblast differentiation has been established, its role in osteoclast differentiation remains unclear. Here we show that B7–H3 is highly expressed in mature osteoclasts and that B7–H3 deficiency leads to the inhibition of osteoclastogenesis in human osteoclast precursors (OCPs). High-throughput transcriptomic analyses reveal that B7–H3 inhibition upregulates IFN signaling as well as IFN-inducible genes, including IDO. Pharmacological inhibition of type-I IFN and IDO knockdown leads to reversal of B7–H3-deficiency-mediated osteoclastogenesis suppression. Although synovial-fluid macrophages from rheumatoid-arthritis patients express B7–H3, inhibition of B7–H3 does not affect their osteoclastogenesis. Thus, our findings highlight B7–H3 as a physiologic positive regulator of osteoclast differentiation and implicate type-I IFN–IDO signaling as its downstream mechanism.

scholarly journals Type I Interferon Upregulates Bak and Contributes to T Cell Loss during Human Immunodeficiency Virus (HIV) Infection

2013 ◽  
Vol 9 (10) ◽  
pp. e1003658 ◽  
Author(s):  
Joseph A. Fraietta ◽  
Yvonne M. Mueller ◽  
Guibin Yang ◽  
Alina C. Boesteanu ◽  
Donald T. Gracias ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Hiv Infection ◽  
Type I Interferon ◽  
Cell Loss ◽  
Type I ◽  
Immunodeficiency Virus

scholarly journals The relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis

2010 ◽  
Vol 69 (Suppl 2) ◽  
pp. A14-A15
Author(s):  
R M Thurlings ◽  
M Boumans ◽  
J Tekstra ◽  
K Vos ◽  
D M van Westing ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Type I Interferon ◽  
Type I ◽  
Interferon Signature ◽  
The Relationship

Type I interferon is induced by hemolysis and drives antibody-mediated erythrophagocytosis in sickle cell disease

Blood ◽  
2021 ◽  
Author(s):  
Yunfeng Liu ◽  
Mouli Pal ◽  
Weili Bao ◽  
Patricia Shi ◽  
Cheryl Lobo ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Type I Interferon ◽  
Type I ◽  
Cell Disease ◽  
Iκb Kinase ◽  
Inducible Genes ◽  
Classical Monocytes

Patients with sickle cell disease (SCD) suffer from intravascular hemolysis associated vascular injury and tissue damage. Classical monocytes (CMo), which are the most abundant of circulating monocytes, are activated in SCD, but the cause and consequences of activation remain incompletely understood. We found a positive correlation between total plasma heme levels and circulating IFN-α in patients with SCD along with upregulation of the type I Interferon (IFN-I) inducible genes in sort-purified SCD patients' CMo by transcriptome analysis. We demonstrated that hemolysis led to IFN-I expression, predominantly by mouse liver monocyte and macrophages (Mϕ), primarily through Tank kinase binding 1 (TBK1)/IκB kinase-ε (IKKε) but not TLR4. In response to hemolysis-induced IFN-I, mouse CMo migrated to the liver and differentiated into monocyte derived Mϕ, increasing their numbers by 6-fold with acute hemin treatment. Hemolysis-driven IFN-I activity also led to the induction of Fc receptor CD64 expression on monocyte and Mϕ populations, enhancing alloantibody-mediated erythrophagocytosis in SCD both in vivo in mice and in in vitro human cultures. Altogether, these data demonstrate IFN-I response to hemolysis as a novel activation pathway in monocytes and Mϕ in SCD, opening the possibility for development of IFN-I-based diagnostics and therapeutics against alloantibody-mediated erythrophagocytosis.

scholarly journals Sunlight exposure exerts immunomodulatory effects to reduce multiple sclerosis severity

2020 ◽  
Author(s):  
Patrick Ostkamp ◽  
Anke Salmen ◽  
Beatrice Pignolet ◽  
Dennis Goerlich ◽  
Till F. M. Andlauer ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Immune Cell ◽  
Type I Interferon ◽  
Disease Risk ◽  
Sun Exposure ◽  
Type I ◽  
Interferon Β ◽  
Sun Sensitivity ◽  
The Relationship ◽  
Reduced Risk

Background: Multiple sclerosis (MS) disease risk is associated with reduced sun exposure. This study assessed the relationship between measures of sun-exposure (vitamin D (vitD), latitude) and MS disease severity, the mechanisms of action, and effect-modification by medication and sun-sensitivity associated MC1R variants. Methods: Two multi-center cohort studies (nNationMS=946, nBIONAT=991). Outcomes were the multiple sclerosis severity score (MSSS) and the number of Gd-enhancing lesion (GELs). RNAseq of four immune cell populations before and after UV-phototherapy of five MS patients. Results: High serum vitD was associated with reduced MSSS (PNationMS=0.021; PBIONAT=0.007) and reduced risk for disease aggravation (PNationMS=0.032). Low latitude was associated with higher vitD, lower MSSS (PNationMS=0.018), fewer GELs (PNationMS=0.030) and reduced risk for aggravation (PNationMS=0.044). The influence of latitude on disability seemed to be lacking in the subgroup of interferon-β treated patients (interaction-PBIONAT=0.042, interaction-PNationMS=0.053). In genetic analyses, carriers of MC1R:rs1805008(T), who reported increased sensitivity towards sunlight (PNationMS=0.038), the relationship between latitude und the number of GELs was inversed (PNationMS=0.001). Phototherapy induced a vitD and type I interferon signature that was most apparent in the transcriptome of monocytes (P=1x10-6). Conclusion: VitD is associated with reduced MS severity and disease aggravation. This is likely driven by sun-exposure, as latitude also correlated with disability and serum vitD. However, sun-exposure might be detrimental for sun-sensitive patients. A direct induction of type I interferons through sun-exposure could explain a reduced effect of latitude in interferon-β treated patients. This could also explain opposite effects of sun-exposure in MS and the type I interferon and sun-sensitivity-associated disease Lupus.

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