Autoimmune Responses and the Roles of Virus Infections, Complimentary Peptides, Phosphatidylserine and Physiologic Checkpoint Molecules in their Generation
Abstract
When there are two complimentary peptides on the class I major histocompatibility (MHC) complexes present on a cell’s surface and the foreign peptide present on a virus binds to a complimentary peptide on the class I MHC of one of them this will produce both an adaptive, and an innate autoimmune response. The adaptive response will be to the foreign virus peptide exposed on the class I MHCs of the infected cells and the innate autoimmune response will be to the self-peptide exposed on the uninfected cells that are complimentary to the peptide the virus binds to. The cytotoxic T cells (CTLs) generated in adaptive immune responses will have peptides on their T cell receptors (TCRs) that are complimentary to the foreign peptide exposed on the class I MHC of the infected cells and to the identical self-peptides on the class I MHCs of uninfected cells.
When there are two complimentary peptides on the class I major histocompatibility (MHC)complexes present on a cell’s surface and the foreign peptide present on a virus binds to a complimentary peptide on the class I MHC of one of them and infects it this will produce both an adaptive immune response to those cells and complimentary peptides on the T cell receptors (TCRs) of the cytotoxic T cells (CTLs) generated there will bind to to the , immune response to the and an innate autoimmune response.
The adaptive response will be to the foreign virus peptide exposed on the class I MHCs of the infected cells and the innate autoimmune response will be to the self-peptide exposed on the uninfected cells that are complimentary to the peptide the virus binds to. The cytotoxic T cells (CTLs) generated in adaptive immune responses will have peptides on their T cell receptors (TCRs) that are complimentary to the foreign peptide exposed on the class I MHC of the infected cells and to the identical self-peptides on the class I MHCs of uninfected cells.
Cells are damaged in all three immune responses resulting in phosphatidylserine (PS) on their surface where it.
References
Michael A Paley, Daniela C Kroy, Pamela M Odorizzi, Jonathan B Johnnidis, Douglas V Dolfi, Burton E Barnett, Elizabeth K Bikoff, Elizabeth J Robertson, Georg M Lauer, Steven L Reiner, E John Wherry (2012) Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection. 338(6111), 1220-5.
Nishi C, Toda S, Segawa K, Nagata S (2014) Tim4- and MerTK-mediated engulfment of apoptotic cells by mouse resident peritoneal macrophages. 34, 1512-20.
Ning Wu, Vitalij Cernysiov, Dominique Davidson, Hua Song, Jianlong Tang, Shanshan Luo, Yan Lu, Jin Qian, Ivayla E. Gyurova, Stephen N. Waggoner, Vincent Quoc-Huy Trinh, Romain Cayrol, Ayumu Sugiura, Heidi M. McBride, Jean-François Daudelin, Nathalie Labrecque, André Veillette (2020) Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation. 30(4), 1129-1140.e5.
Annette Draeger, Roman Schoenauer, Alexander P. Atanassoff, Heidi Wolfmeier, Eduard B. Babiychuk (2014) Dealing with damage: Plasma membrane repair mechanisms. 107(Part A), 66-72.
Jun Suzuki, Toshihiro Fujii, Takeshi Imao, Kenji Ishihara, Hiroshi Kuba, Shigekazu Nagata (2013) Calcium-dependent Phospholipid Scramblase Activity of TMEM16 Protein Family Members. 288(19), 13305-13316.
Downloads
- Article PDF
- TEI XML Kaleidoscope (download in zip)* (Beta by AI)
- Lens* NISO JATS XML (Beta by AI)
- HTML Kaleidoscope* (Beta by AI)
- DBK XML Kaleidoscope (download in zip)* (Beta by AI)
- LaTeX pdf Kaleidoscope* (Beta by AI)
- EPUB Kaleidoscope* (Beta by AI)
- MD Kaleidoscope* (Beta by AI)
- FO Kaleidoscope* (Beta by AI)
- BIB Kaleidoscope* (Beta by AI)
- LaTeX Kaleidoscope* (Beta by AI)
Published
Issue
Section
License
Copyright (c) 2023 Authors and Global Journals Private Limited
This work is licensed under a Creative Commons Attribution 4.0 International License.
