Lecture 44 Flashcards
What is the MHC I antigen presentation pathway?
The internal foreign protein is broken down by the proteasome into peptides, it then travels into the endoplasmic reticulum via TAP and is attached to the MHC-I binding site by the chaperone, then this MHC-I with antigen is moves onto the cell membrane.
What is the MHC-II antigen presenting pathway?
MHC-II is made in the endoplasmic reticulum and has an invarient chain protein attached to the binding site. From there the MHC-II moves into the phagolysosome where it will interact with antigen peptides which were broken down from antigen proteins in the phagolysosome, these will swap places with the invarient chain (li). Once the antigen peptide is attached the MHC-II moves to the cell membrane.
What is odd about MHC-II in regard to virus particles/virus infected cells for antigen presenting cells? What does this allow and where does the primary antigen presenting cell go to do this?
The dendritic cells are able to display viral peptides via MHC-II, virus peptides would normally be shown on MHC-I due to it being endogenous, in dendritic cells howeve they can phagocytose the virus and hence display it on the MHC-II. This allows the activation of T helper T cells during a viral infection. Once the dendritic cells have an antigen to present they travel through the skin to lymphatic vessels which will arrive in the lymph nodes and allows meeting with T cells.
What are T cells?
Lymphocytes (lymphoids) which arise in the bone marrow and fully develop in the thymus. These T cells express T cell receptor (TCR) and co receptors (either CD4 or CD8) which allow them to recognise MHC / peptide complexes.
Where is the thymus? Where do they enter and leave?
The thymus is found roughly above the heart, the bottom lobe is where the immature T cells enter and are screened, the other side is where they leave.
How do T cells become specific? What happens if they end up targeting us? What does the uniqueness of all the T cells mean?
T cells will express a unique T cell receptor produced by random reshuffling or removal or parts of the T cell receptor gene. If this random reshuffling leads to T cell receptors which target our cells or are useless they are destroyed with no second chance. We have billions of possible TCR combinations and as such most T cells will never see use by our immune system, but they are still there just in case.
What are the functions of the two types of T cells?
CD4+ T cells release cytokines which act as a second required signal for activation of either naive B or T cells when they come in contact with their antigen peptide on MHC-II molecules. This helps lower the chance of autoimmunity.
CD8+ T cells become cytotoxic T cells upon recieving cytokines from CD4+ T cells and come in contact with their specific MHC-I molecule. These cytotoxic T cells can destroy virus infected or cancer cells which display their MHC-I antigen by secreting enzymes which cause the affected cell to kill itself by destroying RNA, DNA and other materials, leading to apoptosis of the cell.
What is an APC?
An antigen presenting cell.
What are the other names for unactivated or activated T cells?
Unactivates T cells are known as naive T cells, activated T cells are known as effector T cells.
Why are CD4+ T cells known as helper cells?
They help CD8 T cells become cytotoxic and B cells produce antibodies via production of cytokines.
What is a disease which preys on CD4+ T cells? What does this lead to?
HIV acts on CD4+ cells, this leads to insufficient CD4+ T cells and hence the other adaptive immune system cells can’t act, leading to a weakened immune system.
What are memory T cells?
T cells formed during clonal selection as well as the effector T cells. These memory T cells last for years in our system if not longer and exist in both CD4 and CD8 forms, these memory T cells will become effectors much faster than naive T cells due to not requiring a signal from CD4+.
What are natural killer cells? How do they work and why?
A cell from the lymphoid (lymphocyte) lineage, they don’t have a T cell receptor and instead kill cells with low or absent levels of MHC-I (could be tumour or virus infected). This is done because viruses have coevolved with us and as such have found ways to down regulate MHC-I production to increase survival chance, the natural killer cells exist to counteract this.
