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This antigen presentation pathway enables the immune system to detect transformed or infected cells displaying peptides from modified-self (mutated) or foreign proteins. [ 5 ] [ 6 ] In the presentation process, these proteins are mainly degraded into small peptides by cytosolic proteases in the proteasome , but there are also other cytoplasmic ...
It is in this way, the MHC class I-dependent pathway of antigen presentation, that the virus infected cells signal T-cells that abnormal proteins are being produced as a result of infection. The fate of the virus-infected cell is almost always induction of apoptosis through cell-mediated immunity, reducing the risk of infecting neighboring ...
It is considered to be a stage of antigen presentation pathways. This process involves two distinct pathways for processing of antigens from an organism's own (self) proteins or intracellular pathogens (e.g. viruses ), or from phagocytosed pathogens (e.g. bacteria ); subsequent presentation of these antigens on class I or class II major ...
It is unclear how exactly having the HLA-B27 tissue type increases the risk of ankylosing spondylitis and other associated inflammatory diseases, but mechanisms involving aberrant antigen presentation or T cell activation have been hypothesized. Tissue allorecognition: MHC molecules in complex with peptide epitopes are essentially ligands for TCRs.
Antigen presentation stimulates immature T cells to become either mature "cytotoxic" CD8+ cells or mature "helper" CD4+ cells. An antigen-presenting cell (APC) or accessory cell is a cell that displays an antigen bound by major histocompatibility complex (MHC) proteins on its surface; this process is known as antigen presentation.
In humans, the MHC class II protein complex is encoded by the human leukocyte antigen gene complex (HLA). HLAs corresponding to MHC class II are HLA-DP, HLA-DM, HLA-DOA, HLA-DOB, HLA-DQ, and HLA-DR. Mutations in the HLA gene complex can lead to bare lymphocyte syndrome (BLS), which is a type of MHC class II deficiency.
Once the exogenous antigen peptide is loaded onto the MHC class I molecule, the complex is exported to the cell surface for antigen cross presentation. There is also evidence that suggest that cross-presentation requires a separate pathway in a proportion of CD8(+) dendritic cells that are able to cross-present.
Due to the antigen necessity for MR1 stabilization. MR1 binds the intermediates of riboflavine synthesis. Many human cells can present antigens via MR1 with varying efficiency. [10] [11] [12] Human body can't synthesize most of the vitamins, thus the presence of intermediates of riboflavin synthesis is a marker of non-self