Class I transactivator, NLRC5: a central player in the MHC class I pathway and cancer immune surveillance
Autor: | Saptha Vijayan, Tabasum Sidiq, Peter J. van den Elsen, Koichi Kobayashi, Suhail Yousuf |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
biology MHC class I antigen Histocompatibility Antigens Class I Immunology MHC Class I Gene Intracellular Signaling Peptides and Proteins chemical and pharmacologic phenomena Acquired immune system Major histocompatibility complex Cell biology MHC Class II Gene 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Gene Expression Regulation Neoplasms MHC class I Trans-Activators Genetics biology.protein CIITA Humans CD8 030215 immunology |
Zdroj: | Vijayan, S, Sidiq, T, Yousuf, S, van den Elsen, P J & Kobayashi, K S 2019, ' Class I transactivator, NLRC5: a central player in the MHC class I pathway and cancer immune surveillance ', Immunogenetics, vol. 71, no. 3, pp. 273-282 . https://doi.org/10.1007/s00251-019-01106-z |
ISSN: | 1432-1211 0093-7711 |
Popis: | Major histocompatibility complex (MHC) class I and class II molecules play critical roles in the activation of the adaptive immune system by presenting antigens to CD8+ and CD4+ T cells, respectively. Although it has been well known that CIITA (MHC class II transactivator), an NLR (nucleotide-binding domain, leucine-rich-repeat containing) protein, as a master regulator of MHC class II gene expression, the mechanism of MHC class I gene transactivation was unclear. Recently, another NLR protein, NLRC5 (NLR family, CARD domain-containing 5), was identified as an MHC class I transactivator (CITA). NLRC5 is a critical regulator for the transcriptional activation of MHC class I genes and other genes involved in the MHC class I antigen presentation pathway. CITA/NLRC5 plays a crucial role in human cancer immunity through the recruitment and activation of tumor killing CD8+ T cells. Here, we discuss the molecular function and mechanism of CITA/NLRC5 in the MHC class I pathway and its role in cancer. |
Databáze: | OpenAIRE |
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