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Lecture 9

IMM250 Lecture 9 Notes

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Michael Ratcliffe

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IMM250 Lecture 9 – Effector T cells Slide 3 – Adaptive immunity  The adaptive immune system is an antigen specific response driven by lymphocytes that respond to antigen, which results in the development of immunological memory.  Variable means different types of adaptive immune responses can be generated. The adaptive immune improves over time whereas the innate immune system goes off at the beginning of an infection and stops.  White blood cells called B lymphocytes and T lymphocytes make up the adaptive immune system. B lymphocytes will clonally expand after they are triggered by antigen. The clones are all identical to the original antigen-specific B cell and will secrete antibodies. T lymphocytes will clonally expand after they are triggered by antigen. The clones will resemble the initial antigen responsive cell. The clones will become effector T cells. T cells secrete other molecules such as cytokines and molecules that can directly kill targets. Slide 4 – Acquired immunity  Acquired immunity is the combination of a humoral immune response characterized by the secretion of antibodies and cellular immune response driven by lymphocytes (T cells) and dendritic cells. Dendritic cells are cells of the innate immune system but are good at triggering an adaptive immune response. Dendritic cells bridge the innate and adaptive immune system.  In many cases, the humoral immune system is not enough to clear an infection. In many cases, you also need cell-mediated immunity.  Dr. Watts talked about cell-mediated immunity in response to flu. Vaccines only elicit humoral immunity, but if we can get a vaccine that can elicit cell-mediated immunity, we would have good long term protection. Slide 5 – Adaptive immune responses  Are distinct from innate and non-adaptive phases of immunity, which are not mediated by clonal selection o Innate immunity is not driven by a specific antigen but rather a danger signal  Diversity o By a process of gene recombination to generate a large array of unique antigen receptors  Self/non-self discrimination o This can become disregulated in autoimmune disease  Self limitation o Once the infection is clear, the antigen-specific lymphocytes will contract and die. The immune cells cannot be over-represented by a single clone. The majority of the lymphocytes die off and left with a small population of memory cells. Slide 6 – Antigens  Antigens are foreign proteins that are displayed by a pathogen recognized  B cells and T cells see these in different ways Slide 7 – Antigens  Any substance that can bind to a specific antibody. o They also can be displayed by MHC and recognized by T cells.  Epitope: The structural component of the antigen actually recognized by an antibody and antigen receptor (a.k.a. antigenic determinant). o It is the way the antigen looks to the BCR or TCR.  Many pathogens display multiple epitopes resulting in a polyclonal immune response. o Some epitopes are more dominant than the others. We make immune responses to the best antigens.  Polyclonal response: Response induced by multiple epitopes involves multiple clones of different specificities. o During immunization or infection, many types of B cells and T cells respond to the pathogen because many epitopes displayed by pathogen. The immune response will be specific and hit different aspects of the pathogen. This is a good way of clearing a pathogen. Slide 8 – Poliovirus particle  The blue protein has three epitopes which have a different amino acid sequence so they are recognized by different T cells.  One of the viral proteins showing several peptides, located on the surface of the virus particle, has three peptides that can be recognized by T cells. T cells will be specific for the three epitopes if they are present in your repertoire. You get a polyclonal response to the three epitopes and the individual epitopes of the pink and yellow protein that then expand. Slide 10 – B cells and T cells “see” antigens differently  T cell recognizes a linear epitope in the context of MHC. They recognize an antigen by the variable region of the alpha chain and beta chain domain. T cell receptor only has one binding site. T cell receptor does not get secreted. T cell always stays at the surface of the T cell.  B cells recognize a conformational epitope generated by the tertiary structure of the protein. They recognize the conformational epitopes by a unique binding site that is formed by the heavy and light chain of the variable region of antibody molecule. This confers B cell receptor specificity. When the B cell is activated, the transmembrane of the antibody molecule is removed so it can be secreted as a soluble antibody molecule. This is what is detected in the serum of someone actively fighting an infection or has seen an infection in the past. Slide 11  B cell antibody molecule sticks to the conformational epitope and eliminates the pathogen using a variety of mechanisms (complement, accessory cell, etc.).  T cell epitopes are buried inside the pathogen. This is a good way for the immune system to access protein determinants within a pathogen that do not mutate readily. The surface proteins of influenza mutate a lot, which is why B cell response is seasonal. B cell response has to change every time the virus mutates. The internal proteins do not mutate so much or else it would compromise the fitness of the virus. This is why a vaccine that elicits T cell response for influenza is better. Slide 12 – Recognition of antigen by T cells  MHC molecule o MHC is present on APC. Dendritic cell are the best APC that we have for presenting peptide antigen to T cells.  T cell antigens = peptides o APC gets infected with virus. The virus gets chopped up and peptides are made. The peptides are loaded onto the MHC molecule. The T cell receptor sees the peptide presented on the surface of the APC through the MHC molecule. Slide 14 – Virally infected cell  The degraded viral protein are transported to the ER where it gets associated with MHC (exported out to the surface). This is where recognition takes place with the T cell receptor. Slide 15 – Clonal selection of antigen-specific T cells  The T cell gets activated. The antigen specific T cell will expand. The antigen specific T cells make several daughter cells that have the same TCR as the originating T cell. The daughter cells have the same TCR as the original T cell. They will secrete proteins like cytokines that will help clear the infection. This is the clonal selection hypothesis. Slide 18 – Development and diversification of T cells  The TCR is formed by combining a number of gene segments called VDJ recombination. This is a random process. Slide 19 – T cell receptor (TCR)  The TCR does not have different classes. The TM region allows it to be anchored to the plasma membrane. The plasma membrane of a lymphocyte is a hydrophobic lipid bilayer. The TM region of the TCR is hydrophobic. Slide 20 – T cell co-receptors  CD3 o Quaternary structure o This is important for mediating the signal transmission to the T cell  TCR does not act alone after T cell activation.  TCR has a co-receptor that sits inside the T cell, crosses the TM region and binds to MHC (not the peptide antigen). This is not a variable protein like the TCR. Everyone has the same co- receptors. The co-receptors are one of two different kinds. There is a CD4 and CD8 co-receptor. CD stands for cluster differentiation. A T cell that expresses CD4 behaves differently than a T cell that expresses CD8. A T cell cannot express both, but only one. Slide 21 – T cell co-
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