scholarly journals Restriction factors in human retrovirus infections and the unprecedented case of CIITA as link of intrinsic and adaptive immunity against HTLV-1

Retrovirology ◽  
2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Greta Forlani ◽  
Mariam Shallak ◽  
Elise Ramia ◽  
Alessandra Tedeschi ◽  
Roberto S. Accolla
Keyword(s):  
Adaptive Immunity ◽  
Mhc Class Ii ◽  
Molecular Mechanisms ◽  
Dual Function ◽  
Main Body ◽  
Virus Infections ◽  
Restriction Factors ◽  
Intrinsic Immunity ◽  
Retroviral Replication ◽  
Mhc Class Ii Transactivator

Abstract Background Immunity against pathogens evolved through complex mechanisms that only for sake of simplicity are defined as innate immunity and adaptive immunity. Indeed innate and adaptive immunity are strongly intertwined each other during evolution. The complexity is further increased by intrinsic mechanisms of immunity that rely on the action of intracellular molecules defined as restriction factors (RFs) that, particularly in virus infections, counteract the action of pathogen gene products acting at different steps of virus life cycle. Main body and conclusion Here we provide an overview on the nature and the mode of action of restriction factors involved in retrovirus infection, particularly Human T Leukemia/Lymphoma Virus 1 (HTLV-1) infection. As it has been extensively studied by our group, special emphasis is given to the involvement of the MHC class II transactivator CIITA discovered in our laboratory as regulator of adaptive immunity and subsequently as restriction factor against HIV-1 and HTLV-1, a unique example of dual function linking adaptive and intrinsic immunity during evolution. We describe the multiple molecular mechanisms through which CIITA exerts its restriction on retroviruses. Of relevance, we review the unprecedented findings pointing to a concerted action of several restriction factors such as CIITA, TRIM22 and TRIM19/PML in synergizing against retroviral replication. Finally, as CIITA profoundly affects HTLV-1 replication by interacting and inhibiting the function of HTLV-1 Tax-1 molecule, the major viral product associated to the virus oncogenicity, we also put forward the hypothesis of CIITA as counteractor of HTLV-1-mediated cancer initiation.

scholarly journals MHC Class II Transactivator Is an In Vivo Regulator of Osteoclast Differentiation and Bone Homeostasis Co-opted From Adaptive Immunity

2014 ◽  
Vol 29 (2) ◽  
pp. 290-303 ◽  
Author(s):  
Elisa Benasciutti ◽  
Elisabetta Mariani ◽  
Laura Oliva ◽  
Maria Scolari ◽  
Egon Perilli ◽  
...  
Keyword(s):  
Adaptive Immunity ◽  
Mhc Class Ii ◽  
Osteoclast Differentiation ◽  
Class Ii ◽  
Bone Homeostasis ◽  
Class Ii Transactivator ◽  
Mhc Class Ii Transactivator

scholarly journals Bridging autoinflammatory and autoimmune diseases

2021 ◽  
Vol 33 (1) ◽  
Author(s):  
Emad M. El-Shebiny ◽  
Enas S. Zahran ◽  
Sabry A. Shoeib ◽  
Eman S. Habib
Keyword(s):  
Innate Immunity ◽  
T Lymphocytes ◽  
Autoimmune Diseases ◽  
Adaptive Immunity ◽  
High Titre ◽  
The Other ◽  
Clinical Spectrum ◽  
Autoinflammatory Diseases ◽  
Main Body ◽  
B And T Lymphocytes

Abstract Background Autoimmunity is used to cause by impairment of adaptive immunity alone, whereas autoinflammatory was originally defined as a consequence of unregulated innate immunity. So, the pathogenetic mechanisms of autoimmune diseases were well-thought-out to be mediated by B and T lymphocytes. Whereas, autoinflammatory diseases were defined as unprovoked times of inflammation with the absence of a high titre of autoantibodies. Main body of the abstract Autoimmune and autoinflammatory diseases were split into two groups, but considering the similarities, it can be considered as only one group of diseases with a large immune pathological and clinical spectrum which involves at one end pure autoimmune diseases and the other pure autoinflammatory diseases. Conclusions We can safely conclude that there is bridging between autoinflammatory and autoimmune diseases.

scholarly journals Molecular mechanisms and the vital roles of resistin, TLR 4, and NF-κB in treating type 2 diabetic complications

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Venkataiah Gudise ◽  
Bimalendu Chowdhury
Keyword(s):  
Type 2 Diabetes ◽  
Effective Treatment ◽  
Diabetic Complications ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Vascular Complications ◽  
Diabetic Patients ◽  
Rapid Progression ◽  
Main Body

Abstract Background Type 2 diabetes in obese (≥ 25 and ≥ 30 kg/m2) patients is the foremost cause of cardiovascular complications like stroke, osteoarthritis, cancers (endometrial, breast, ovarian, liver, kidney, colon, and prostate), and vascular complications like diabetic neuropathy, diabetic and retinopathy, and diabetic nephropathy. It is recognized as a global burden disorder with high prevalence in middle-income nations which might lead to a double burden on health care professionals. Hence, this review emphasizes on understanding the complexity and vital signaling tracts involved in diabetic complications for effective treatment. Main body Type 2 diabetes in overweight patients induces the creation of specific ROS that further leads to changes in cellular proliferation, hypothalamus, and fringe. The resistin, TLR4, and NF-κB signalings are mainly involved in the progression of central and fringe changes such as insulin resistance and inflammation in diabetic patients. The overexpression of these signals might lead to the rapid progression of diabetic vascular complications induced by the release of proinflammatory cytokines, chemokines, interleukins, and cyclooxygenase-mediated chemicals. Until now, there has been no curative treatment for diabetes. Therefore, to effectively treat complications of type 2 diabetes, the researchers need to concentrate on the molecular mechanisms and important signaling tracts involved. Conclusion In this review, we suggested the molecular mechanism of STZ-HFD induced type 2 diabetes and the vital roles of resistin, TLR4, and NF-κB signalings in central, fringe changes, and development diabetic complications for its effective treatment. Graphical abstract

scholarly journals Deaminase-Independent Mode of Antiretroviral Action in Human and Mouse APOBEC3 Proteins

2020 ◽  
Vol 8 (12) ◽  
pp. 1976
Author(s):  
Yoshiyuki Hakata ◽  
Masaaki Miyazawa
Keyword(s):  
Molecular Mechanisms ◽  
Restriction Factors ◽  
Mrna Editing ◽  
Antiviral Function ◽  
Apobec3 Proteins ◽  
And Function ◽  
Editing Enzyme ◽  
Dependent Pathway ◽  
Independent Mode ◽  
Human Apobec3g

Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 (APOBEC3) proteins (APOBEC3s) are deaminases that convert cytosines to uracils predominantly on a single-stranded DNA, and function as intrinsic restriction factors in the innate immune system to suppress replication of viruses (including retroviruses) and movement of retrotransposons. Enzymatic activity is supposed to be essential for the APOBEC3 antiviral function. However, it is not the only way that APOBEC3s exert their biological function. Since the discovery of human APOBEC3G as a restriction factor for HIV-1, the deaminase-independent mode of action has been observed. At present, it is apparent that both the deaminase-dependent and -independent pathways are tightly involved not only in combating viruses but also in human tumorigenesis. Although the deaminase-dependent pathway has been extensively characterized so far, understanding of the deaminase-independent pathway remains immature. Here, we review existing knowledge regarding the deaminase-independent antiretroviral functions of APOBEC3s and their molecular mechanisms. We also discuss the possible unidentified molecular mechanism for the deaminase-independent antiretroviral function mediated by mouse APOBEC3.

scholarly journals The MHC Class II transactivator CIITA inhibits the persistent activation of NF-kB by Tax-1

Retrovirology ◽  
2015 ◽  
Vol 12 (S1) ◽  
Author(s):  
Greta Forlani ◽  
Rawan Abdallah ◽  
Luisa Guidali ◽  
Roberto S Accolla ◽  
Giovanna Tosi
Keyword(s):  
Mhc Class Ii ◽  
Class Ii ◽  
Class Ii Transactivator ◽  
Mhc Class Ii Transactivator
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