Terms : Hide Images
| 5798746552 | Antigenic epitopes | B cell epitope: Specific surface piece of antigen or secreted molecule/toxin that antibody binds to. Conformation or linear (RARE). T cell epitope: Specific piece of antigen held by an MHC molecule and used by an APC. MUST be linear. Can be derived from antigen surface or internal. | 0 | |
| 5798746553 | MHC | Major histocompatibility complex Role: Present portions of antigens that are noncovalently bound to MHC gene products, (MHC class I and II molecules) to antigen-specific T cells. Any T cell recognizes foreign antigen bound to only ONE specific MHC class I or II molecule. Class I and II differ in function, tissue distribution, and biochemical composition. | 1 | |
| 5798746554 | MHC & NK cells | NK cells destroy any cells not expressing self-MHC class I without discrimination. | 2 | |
| 5798746555 | MHC Class I | Expressed on most nucleated cells. Restricts antigen recognition by CD8 T cells. | 3 | |
| 5798746556 | MHC Class II | Expressed on professional APCs. Restricts antigen recognition by CD4 T helper cells. | 4 | |
| 5798746557 | Histocompatibility | Recognition of class I or II molecules by T cell receptors. Determines tissue compatibility or incompatibility. | 5 | |
| 5798746558 | Peptide binding cleft | Located at the amino terminal end. Cleft does NOT have fine specificity like antibodies or TCRs; ~2000 different peptides/MHC alleles. | 6 | |
| 5798746559 | MHC Class I structure | Has 2 beta chains. Nearly all nucleated cells present this class. Noncovalently associated. Binding groove is CLOSED. Bound peptides are 8-10 AAs in length. Anchor residues: Specific AAs essential for binding peptides to a particular class I molecule. These sets of peptides have the same or similar AA residues at several defined positions. These common AA signatures bind the peptide into the MHC groove. | 7 | |
| 5798746560 | 8 | |||
| 5798746561 | MHC Class II structure | Generally only expressed by APCs. Has 1 alpha and 1 beta chain. Cleft is open at BOTH ends. Bind peptides 10-30 AAs in length. Lack anchor residues; binding peptides have internal conserved "motifs" | 9 | |
| 5798746562 | Capture of antigens | 1: Pathogen enters through various epithelium 2: Professional APCs are in these tissues and take up/process antigen 3: Professional APCs migrate into draining lymph nodes via afferent vessels 4: After MHC-TCR engagement, antigen-specific T cells proliferate, take on effector functions, and migrate to the site of infection via efferent vessel EXCEPTION: Blood borne pathogens filter through the spleen | 10 | |
| 5798746563 | Cytosolic pathway - MHC class I peptide loading | 1: Ubiquitination of protein; proteins become target of proteasomes, which chop up proteins into peptides. 2: TAP uses ATP to translocation peptides into the ER lumen. 3: Tapasin links empty class I, which is held in the correct confirmation by chaperones, to TAP for easy access to incoming peptides. 4: Peptides fit into the binding cleft cause the release of chaperones. 5: Result is stable MHC -- peptide is transported to the surface via Golgi. | 11 | |
| 5798746564 | Endocytic pathway - MHC Class II peptide loading | 1: MHC Class II molecules are constantly made and assembled in the ER. 2: Chaperones bring alpha and beta proteins together and held together with I, the invariant chain. 3: MHC Class II with the invariant chain are transported through the Golgi to MIIC, the MHC class II compartment. 4: Extracellular protein gets taken up by APC Into endosomes. Proteins become target of proteasomes within the endosomes as pH drops. 5: Proteosomes chop up the antigenic proteins into peptides in endosomes, which then fuse with MIIC. 6: Enzymes digest the invariant chain leaving only CLIP (Class II invariant chain peptide) in the presence of free antigenic peptides. 7: HLA-DM assists in the replacement of CLIP with antigenic peptide. 8: Formation of stable MHC II: Peptide is then transferred to the surface for recognition by specific TCR. | 12 | |
| 5798746565 | Cross-presentation | Peptides derived from the extracellular environment or from within endosomes/lysosomes get redirected into the cytosolic pathway for presentation by MHC Class I. | 13 | |
| 5798746566 | Why does cross presentation occur? | Non-professional APCs may become unable to properly present antigen to CD8 T cells upon infection with pathogens. Dendritic cells can ingest these infected cells and stimulate helper T cells and cytotoxic Ts. | 14 | |
| 5798746567 | CDI antigen presentation | MHC-like, but not polymorphic. Associates with Beta 2m. Involved in presentation of lipid antigens, a major constituent of some pathogens. | 15 | |
| 5798746568 | Dendritic cells | Constitutively high in MHC II and costimulatory activity. | 16 | |
| 5798746569 | Macrophages | Must be activated for high MHC II and costimulatory molecules. | 17 | |
| 5798746570 | B cells | Constitutively MHC II, but activated for costimulatory molecules. | 18 | |
| 5798746571 | Why must T cells recognize MHC + antigen? | Proximity: CD4 T cells, B cells, CD7 T cells, infected cells. Less saturation: If TCRs were saturated with free antigen, specific killing of target cells would be inhibited. Restriction: T cells see and respond only to cell associated antigen. Eliminates non-specific killing. 2 pathways; Best protection skewed to individual pathogens. Viruses and extracellular bacteria get different responses. | 19 | |
| 5798746572 | How does the MHC haplotype determine diste susceptibility? | MHC are a complex of linked multiallelic genes located on one chromosome that code for molecules that restrict specificity of antigen recognition by T cells. MHC can determine disease susceptibility or resistance in a given host. | 20 | |
| 5798746573 | Why is there an enormous allotropic variation of MHC molecules? | All immune systems are different, so the perfect pathogen cannot evolve to spread through a population. It may be less likely for a microbe to imitate if there is a larger variety of MHC. | 21 |
