ArticleFrontiers in microbiology2013
The MHC-II transactivator CIITA, a restriction factor against oncogenic HTLV-1 and HTLV-2 retroviruses: similarities and differences in the inhibition of Tax-1 and Tax-2 viral transactivators.
Article in Frontiers in microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Correspondence on editorial regarding "Novel role of MHC class II transactivator in hepatitis B virus replication and viral counteraction".Clinical and molecular hepatology · 2024Article
- Class II transactivator restricts viral replication, extending its effect to HBV: Editorial on "Novel role of MHC class II transactivator in hepatitis B virus replication and viral counteraction".Clinical and molecular hepatology · 2024Article
- The NLR member CIITA: Master controller of adaptive and intrinsic immunity and unexpected tool in cancer immunotherapy.Biomedical journal · 2023Review
- Hijacking Host Immunity by the Human T-Cell Leukemia Virus Type-1: Implications for Therapeutic and Preventive Vaccines.Viruses · 2022Review
- Review
- Restriction factors in human retrovirus infections and the unprecedented case of CIITA as link of intrinsic and adaptive immunity against HTLV-1.Retrovirology · 2019Review
- HTLV-1 HBZ Protein Resides Exclusively in the Cytoplasm of Infected Cells in Asymptomatic Carriers and HAM/TSP Patients.Frontiers in microbiology · 2019Article
- HTLV Deregulation of the NF-κB Pathway: An Update on Tax and Antisense Proteins Role.Frontiers in microbiology · 2018Review
- Article
- Tripartite Motif-Containing Protein 22 Interacts with Class II Transactivator and Orchestrates Its Recruitment in Nuclear Bodies Containing TRIM19/PML and Cyclin T1.Frontiers in immunology · 2017Article
- HTLV-1 HBZ Viral Protein: A Key Player in HTLV-1 Mediated Diseases.Frontiers in microbiology · 2017Article
- Tripartite Motif 22 and Class II Transactivator Restriction Factors: Unveiling Their Concerted Action against Retroviruses.Frontiers in immunology · 2017Review
- Cytoplasmic Localization of HTLV-1 HBZ Protein: A Biomarker of HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP).PLoS neglected tropical diseases · 2017Article
- The MHC-II transactivator CIITA inhibits Tat function and HIV-1 replication in human myeloid cells.Journal of translational medicine · 2016Article
- The Major Histocompatibility Complex Class II Transactivator CIITA Inhibits the Persistent Activation of NF-κB by the Human T Cell Lymphotropic Virus Type 1 Tax-1 Oncoprotein.Journal of virology · 2016Article
- Editorial to the Research Topic "Comparative studies between HTLV-1 and HTLV-2 function and pathobiology".Frontiers in microbiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of CD4(+) T helper cells is strictly dependent on the presentation of antigenic peptides by MHC class II (MHC-II) molecules. MHC-II expression is primarily regulated at the transcriptional level by the AIR-1 gene product CIITA (class II transactivator). Thus, CIITA plays a pivotal role in the triggering of the adaptive immune response against pathogens. Besides this well known function, we recently found that CIITA acts as an endogenous restriction factor against HTLV-1 (human T cell lymphotropic virus type 1) and HTLV-2 oncogenic retroviruses by targeting their viral transactivators Tax-1 and Tax-2, respectively. Here we review our findings on CIITA-mediated inhibition of viral replication and discuss similarities and differences in the molecular mechanisms by which CIITA specifically counteracts the function of Tax-1 and Tax-2 molecules. The dual function of CIITA as a key regulator of adaptive and intrinsic immunity represents a rather unique example of adaptation of host-derived factors against pathogen infections during evolution.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.