BMS 300 1st edition Lecture 37Outline of Last Lecture I. The spleen, macrophages, and red pulp II. The spleen as organ of the immune system -white pulp and cells of immunity -monitoring for blood borne pathogens III. The formation of lymph -hydrostatic and osmotic pressure -surfeit of extravascular fluid 1. lymph 2. lymph in lymphatic vessels 3. lymph in lymph nodes >germinal regions and cells of immunity >monitoring extracellular space IV. Peyer’s patches, tonsils, and the epithelium -germinal regions and monitoring what enters from the outside V. Thymus -monitor T-lymphocytes for efficacy and specificityVI. Types of immunity -innate/non-specific These notes represent a detailed interpretation of the professor’s lecture. Grade Buddy is best used as a supplement to your own notes, not as a substitute.-adaptive/specific VII. Branch’s system -humoral -cellular VIII. Cells of immunity Outline of Current Lecture IX. Types of immunity and the cell types involved -innate/non-specific 1. rapid, short-term, non-specific, memory 2. two forms >humoral -secreted antibody >cellular -T-cell receptors as transmembrane proteins X. Cells of immunity-innate—granulocytes 1. neutrophils 2. Eosinophils 3. basophils -adaptive 1. lymphocytes >B lymphocytes—humoral>T lymphocytes—cellular -macrophages/ dendritic cells 1. o deratein both systems >processional antigen presenting cells XI. Innate response -interferon—virus -inflammation—bacteria Current LectureInflammation as the innate or non-specific response to bacteria 1. Redness 2. Swelling 3. Heat4. Pain Stratified squamous epithelium-sits on a basal lamina -dermis is right behind it -there are fibrocytes in the dermis but there is a lot of extracellular space in between them -there are also blood vessels (when you bleed) -the capillaries are lined by a continuous layer of endothelial cells -imagine a splinter going into the dermis -the splinter will deposit bacteria into that region -the bacteria begin to replicate and make copies of themselves -some of the bacteria will slough bacterial proteins (sometimes toxins) -there are now proteins in the extracellular space -the proteins become a chemo attractant -the proteins get into the blood vascular compartment and they will find their way to thered bone marrow -in the red bone marrow there is a reservoir of cells called neutrophils (type of granulocyte)-when the bacteria makes their way in the bone marrow there’s a “signal” to have the neutrophils go into the blood vascular compartments-the cells are likely to flow past the site -the toxins affect the endothelial cells -they tell the endothelial cells to put out proteins called selectins on their surface -compliment on the neutrophils (aka the selectins are on the neutrophils as well)-the selectins are sticky for one another (like Velcro)-this causes them to slow down in the blood and move out across the wall -then the process called extravasation begins -at about the same time there is another set of cells called mast cells -mast cells: chocked full of vesicles with histamine in them (histamine releasing cell) -signal them through exocytosis to release histamine -histamine binds to vascular smooth muscle to cause muscle relaxation -around the site where the bacteria is the mast cells are releasing histamine -the histamine can move upstream the blood vessels and cause the smooth muscle to relax -the resistance of the vessel will go down so the blood flow will go up -when you bring more blood you get redness and heat largely resulting from the histamine on the muscle -histamine causes a separation between endothelial cells -the increase blood flow with the wider gaps in between the endothelial cells -there will be fluid coming out of the blood vascular in between the endothelial cells andbuild up fluid that causes swelling -pain is simply the binding of local toxins to pain neurons -meanwhile the neutrophils are causing chaos -the neutrophils are a granulocyte -among the molecules will be hydrogen peroxide and bleach -there will be channels to admit free electrons to be released -they are killing bacteria -kind of a “debris” field -monocyte: immature macrophage -the monocytes are mobilized in the red bone marrow and do all the same things as the neutrophils -the monocytes will mature into macrophages (big eaters) endocytic cells -they clean up the debris and chaos left behind -the monocytes have transmembrane proteins on them that are sticky for bacteria-the signal on them is the signal to begin endocytosis -the bacterium is targeted to the lysosome (garbage disposal of the cell)-the lysosome contains hydrolytic enzymes which convert proteins to peptides (peptide fragments)-when the bacterium arrives the enzymes will convert the bacteria into smaller peptides -there are sites in the endosomes which contain an important transmembrane protein (MHC2 protein) major histocompatibility class 2 protein >in the lysosome or the endosome and binds to the fragment of bacterial protein-the vesicle is delivered to the plasma membrane and undergoes exocytosis (the bacteriaare now on the surface of the cell) -MHC2 protein displaying a fragment of bacterial protein -these proteins are said to make the macrophages a professional antigen presenting cell >macrophages >dendritic >and one more -all of these are antigen presenting cells -the macrophages are basically cleaning up the mess -after they have been on the site for a little while they go back into the blood vascular compartment and head to germinal regions of lymphoid tissue -basically trying to find the specific cell in the immune system to respond -can take up to two weeks to complete the cycle Interferon as the innate response to viral infections (invasion) -flu virus -we have a single layer of epithelial cells that sit on a basal lamina -a virus particle >can’t live on their own -flu virus gains access by a protein called hemoglobin -the virus binds to the receptor and will gain access by exocytosis -which will now allow the virus to be enveloped by a vesicle -then the virus can get out into the cytoplasm -the virus commandeers the protein synthesis machinery of the cell -they then go out into the outside world into the host cell lipid bilayer which has the hemoglobin protein attached on its surface-the viral “escape” requires a viral enzyme called neuraminidase (cleaves sugar molecules) -we name flu viruses as H and N, h=hemoglobin, n=neuraminidase -once
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