Topics to know for Exam 1 PDF

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*Please note that these questions are ONLY a guide. They are NOT actual test questions. Some, all, or none of these topics may be on your exam. Professor Weigel did not view it. All questions are based off of the PowerPoints or lecture recordings. Do NOT use this as your ONLY study resource, continue to review PowerPoints, recordings, textbook, notes, light board videos, etc* Chapter 1 a. What is Immunology? - Immunology is the study of physiological mechanism that are used to defend the body from invasion by foreign or infectious agents. CHPTER 1 PAGE 4 b. Who discovered vaccination? How did he do it? - Edward Jenner discovered the procedure called a vaccination and he did it by inoculating a 8 year old boy with cowpow to find that he was immune to smallpox. CHPTER 1 PAGE 9 b. What are vaccines? Why are they important? - Vaccines is a procedure that is done that prevents severe disease by exposing the immune system to the infectious agent in a weakened or killed state. It provides long term protection against the real pathogen with very little risk of becoming sick. CHPTER 1 PAGE b. What are some differences between innate and adaptive immune systems? (Specificity, cells involved, timing, etc.) - Innate- is the first line of defense against infections, works rapidly, gives rise to the acute inflammatory response, has specificity for microbes and uses different receptors to recognize pathogens - Adaptive- takes longer to develop (7 days), is highly specific for antigens, uses one type of receptors to recognize many different pathogens, primary immune response and secondary immune response CHPTER 1 PAGE 20 b. How does a secondary immune response compare to a primary immune response in terms of response time and effectiveness? - Primary immune response is the first time the adaptive immune system response is activated against a pathogen rather than the secondary immune system which is any time the adaptive immune response is activated against a pathogen that is has been exposed to before CHPTER 1 PAGE 20 c. If you lack adaptive immunity, what will happen? - People lacking adaptive immunity can control the infection but can not clear it CHAPTER 1 PAGE 23 d. If you lack innate immunity, what will happen? - People that are lacking innate immunity can not control the infection at all. Innate immunity cells are needed to activate the adaptive cells. - Chile they die CHAPTER 1 PAGE 23 b. What is a pathogen? What is an opportunistic pathogen?

A pathogen is any organism with potential to cause disease/ (Influenza and typhoid bacillus are examples of what we call a pathogen). - An opportunistic pathogen causes disease is the body’s defenses are weakened or it gets into a part of the body it isn’t normally found. (An example would be E.coli, E.coli is okay to be in the intestines, it is its happy place but when found outside of the intestines it would cause infection.) CHAPTER 1 PAGE 10 What are the 4 types of pathogens that cause disease in humans? - Bacteria (Mycobacterium tuberculosis---Tuberculosis) - Viruses (HIV----AIDS) - Fungi (Candida albicans----Thrush.systemic candidiasis) - Parasite (protozoa----Trypanosoma----Sleeping sickness) - CHAPTER 1 PAGE 11 Which bacteria is gram positive? Which is gram negative? What is special about each? (Example Teichoic/Lipoteichoic acid or LPS / if it retains the purple dye or stains pink, etc.) - Gram- Positives --- Bacillus, Staphylococcus aureus, Steptococcus & Mycobacterium (kinda) TERICHOIC ACIDS & LIPOTEICHOIC ACIDS - Gram-Negative----E.coli, Pseduomonas, salmonella & Shigella LPS - Viruses- HIV, Influenza - MICROBE SHEET What receptors are found on human cells that help recognize pathogens? How about on pathogen cells? (Hint: PRR, PAMP) - PRR = pattern recognition receptors - PAMP = pathogen associated molecular patterns - PRR you would on the surface of your immune system cells - PAMP you would on the surface of pathogens What is the purpose/function of the following cells?  Lymphoid cells – 20-50% of white blood cells, T cells, B cells and NK cells  Mononuclear phagocytes- Monocytes that circulate in the blood & Macrophages are found in the tissue  Granulocytic cells – These are granulocyte —Neutrophils, Eosinophils & Basophils (They are based on morphology and cytoplasmic staining characteristics)  Dendritic cells – Main function is the presentation of antigens to T cells  CHAPTER 1 PAGE 25 What are granulocytes (list all of them) and what are their staining/physical characteristics? (only describe the staining characteristics for B.E.N) - Basophil: granulocytes which stain with basic dyes (blue) also presented in extremely low numbers in the circulation, Basophils & Mast cell are similar in morphology, DARKEST STAINED, Multilobed nucleus & control immune responses to parasites. - Eosinophil: granular leukocytes which stain with eosin (red). SECOND DARKEST STAIN, low levels in circulation, primarily responsible for extracellular killing of large parasites such as worms. - Neutrophil; Phagocytosis and killing of microorganisms, NEURTAL AGAINST RED BLOOD CELLS // LEAST STAINED, effectors of innate immunity and ate specialized in the capture engulfment and killing microbes, Are a part of phagocytic for cells that contain toxic -

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substances in intracellular granules, anaerobic and aerobic envirmont. Short-lived, they are like the marines they go out first when there is an infection. g. What are the 3 lymphocytes and which are involved with the adaptive immune response? - Small lymphocytes (adaptive immunity cells) - B lymphocytes (B cells) - T lymphocytes (T cells) - CHAPTER 1 PAGE 29 h. How are lymphocytes and leukocytes related? - ALL lymphocytes are leukocytes BUT not all leukocytes are lymphocytes. - CHAPTER 1 PAGE 26 i. What is hematopoiesis? Draw the different cell lineages and include the general functions of each cell. (Which cell does not have a nucleus?) - The generation of cellular elements of blood including - Red Blood cells RBC - White Blood Cells WBC or leukocytes - Megakaryocytes- where platelets are formed -

- CHAPTER 1 PAGE 26 Where does hematopoiesis take place? - Bone marrow - Active throughout life because blood cells are both vital and shortlived. - CHAPTER 1 PAGE 48 k. Which cells (monocytes/macrophages) circulate and which reside in tissues? - MONOCYTES circulate in the blood for about 8 hours, then mature and migrate into tissue, they are then referred to as MACROPHAGES. - Both are phagocytic - Monocytes in the peripheral/circulatory blood j.

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- Macrophages in the tissue - CHPTER 1 PAGE 36 What cells are responsible for creating platelets? - Megakaryocytes: is a bone marrow cells responsible to produce blood platelets when its cytoplasm becomes fragmented // the fragments are blood platelets. - CHAPTER 1 PAGE 46 What is another name for red blood cells? - Erythrocytes - They have important immunological role in clearing immune complexes from the circulation in persistent infections and in some autoimmune diseases. - CHAPTER 1 PAGE 47 What is affinity? Why is it important? - Affinity is the measure of the strength with which one molecule binds to another at a single binding site - TEXTBOOK GLOSS What cells create antibodies? What is another name for antibodies? - Effecter B cells secretes antibodies - Another name for antibodies are Immunoglobulins---proteins molecules synthesized by cells of the immune system—part of the humoral immunity (humoral—bodily fluids) - CHAPTER 1 PAGE 56/65 As learned in class, are antibodies secreted or membrane bound? - Antibodies are secreted - CHAPTER 1 PAGE 56 Where do B cells mature? - B cells mature in the bone marrow - CHAPTER 1 PAGE 60 What are the two receptors associated with T cells? (what are the names of the T cells) - T helper cells (TH) – CD4 cell- they help activate other B cells that later become Plasma cells that secrete antibodies IN LYMPH NODE - T cytotoxic cells (TC)-CD8 cell- help fight infectious pathogens - CHAPTER 2 PAGE 31 Where do T cells mature? - T cells mature in the thymus - CHAPTER 1 PAGE 60 Where do T and B cells go once they encounter an antigen? - Lymphocytes (B & T cells) are found in lymphoid tissues, blood and lymph, ACTIVATED in the secondary lymphoid tissues - The meeting place where lymphocytes circulating blood encounter antigens bought from sites of infection is the secondary lymphoid organs?? What is the difference between primary and secondary lymphoid organs? - Primary Lymphoid system: Thymus and bone marrow are primary organs - Maturation occurs in the primary lymphoid organs

Secondary Lymphoid system: Lymph nodes, spleen and mucosalassociated tissues are secondary organs - Which trap antigen and promote lymphocyte activation - Activation occurs in the secondary lymphoid organs What is general structure of a lymph node? Where do the B cells reside within the lymph node? Where do the T cells reside within the lymph node? - Kidney-shaped; packed with lymphocytes & macrophages through which lymph percolates - Lymphocytes leave blood and enter lymph nodes where they are activated by pathogens (draining) What is Phagocytosis? What cells use phagocytosis? - Phagocytosis is the “eating/taking’ up of a pathogen and the process involves (1) the bacterium becomes attached to membrane evaginations called pseudopodia - . (2) Bacterium is ingested forming Phagosome - . (3) Phagosome fuses with lysosomes - . (4) Lysosomal enzymes digest captured material. - (5) Digestion products are releases from cell - Neutrophils, Monocytes and Macrophages use phagocytosis What is Mucosal-Associate Lymphoid Tissue (MALT)? - Mucosal surfaces lining digestive, respiratory and urogenital tracts are the major sites of entry for pathogens and are defended by MALT - MALT are tissues range from loosely organized clusters of lymphoid cells to well-organized structures- tonsils, appendix - Lymphocytes activated in the MALT tend to stay in the MALT and the memory cells serve the MALT in the future - CHAPTER 1 PAGE 70 What are M cells? What do they do? Where are they found? - Pathogens arrive through direct delivery across mucosa mediated by specialized cells called M cells. - M Cells are found in the GALT - CHAPTER 1 PAGE 71 What is red pulp? What is white pulp? What organ is involved? - Red pulp is the filter for blood that removes old or damages cells - White pulp is the site where blood borne pathogens encounter lymphocytes (a secondary lymphoid organ) - These take place in the spleen - CHAPTER 1 PAGE 68 -

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PRR = pattern recognition receptors PAMP = pathogen associated molecular patterns PRR you would on the surface of your immune system cells PAMP you would on the surface of pathogens Ex. PAMP is LPS on Gram neg bacteria Leukocytes = white blood cells 1. Lymphocytes = T-cells, B-cells, and NK cells

T-cell and B-cell adaptive immune response

NK cells innate immune response 2. Granulocytes = BEN Basophils, Eosinophils, Neutrophils Innate immune response Antibodies (ab's) = BCR's (B-cell receptors) = Immunoglobulins (Ig's) IgA ImmunolgobulinA CD4 T-cells and CD8 T-cells B-cells =plasma B-cells and memory B-cells T-cells = CD4 and CD8 Dendritic cells

Chapter 2 / selected topics of Chapter 3 aa. Know the mechanical, chemical, and microbiological protections of the body (ex. The three defense categories)

bb. What is the difference between extracellular versus intracellular pathogens? - Pathogens can infect cells directly (intracellular) or live outside of cells (extracellular) cc. What are the 3 pathways to complement activation? Which one occurs first? Last? - Alternative, Classical and Lectin - Alternative occurs FIRST ( acts right away) - Lectin occurs SECOND ( a couple of hours to a day - Classical occurs LAST (7 days roughly) - THEY ARE ALL UBIQUITOUS dd. What is the purpose of complement?

Tags pathogens and extracellular molecules by phagocytic cells such as macrophages - Can destroy pathogens directly by poking holes in the outer membrane or cell wall with the membrane attack complexes (MAC) ee. What bond binds complement fragments to the pathogen? When does this bond get exposed? - The Thioester bond is what binds complement fragments to the pathogen - The thioester bond is exposed when the cleavage of C3 to C3a and C2b. The cleavage of C3 exposes the thioester bond. Nucleophilic attack then covalently bonds to pathogen ff. What is the soluble C3 convertase and how is it formed? - This process occurs continuously at low rate in blood, lymph and extracellular fluids - Rate increases in vicinity of certain pathogens - iC3 is the product of C3 hydrolysis but there is no cleavage of C3 - iC3 binds to factor B in the blood or ECF making factor B susceptible to cleavage by factor D at pathogen’s surface - iC3Bb is produced (soluble form of C3 convertase) iC3Bb cleaves C3 into C3a and C3b - Some of C3b becomes bound to pathogen’s surface -

gg. What is opsonization? Which complement component can act as an opsonin? - Opsonization is a protein bound to the surface of a pathogen that facilitates its phagocytosis - C3b is a complement component that can act as a opsonin hh. What is the alternative C3 convertase and how is it formed? - Factor B binds to C3b fragments and is cleaved by factor D, the complex of C3bBb is formed on the pathogen‘s surface = C3 convertase of the alternative pathway - Assembly of some C3 convertase molecules results in more C3 being cleaved and more C3b attached to the pathogen’s surface assembly of even more convertase…process of progressive amplification that rapidly coats the pathogen with C3b ii. What receptors bind to what fragments? (CR1, CR3, CR4, etc) - CR1 recognizes C3b (CR1 can also play a protective role by C3 susceptible to face I to iC3b) - CR2 is a B-cell co-receptor and recognizes C3d - CR3 a& CR4 recognize iC3b (iC3b can be recognized by phagocytic cells) jj. What is the classical C3 convertase? The same as alternative but starting out it uses Ig’s or CPR’s and convertases C4 and C2 first kk. Draw out the steps for the Alternative Pathway.

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ll. What is the C5 convertase of the alternative pathway? - Picture mm. What is the C5 convertase of the classical/lectin pathway?

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nn. When C3 or C5 is cut, what happens to the ‘b’ fragments and what happens to the ‘a’ fragments? - C3a and C5a contribute to acute inflammation - Also referred to as anaphylatoxins - C5a is more stable and potent than C3a - What exactly do they do? - bind mast cells, phagocytes and endothelial cells -  release of histamine from mast cells - Histamine increases blood vessel permeability and blood flow - Activate endothelial cells  direct phagocytes to site of infection - The “b” fragment can lead to 3 other components such as opsonization, another conversate and a C5 convertase oo. What is MAC? What does it do? What components does it include? - MAC is a process that can destroy pathogens directly by poking holes in the outer membrane or cell wall with the membrane attach complex - It involves C5b (specifically) – C9 pp. What protein/s stabilize complement fragments and convertases? - Proteins controlling complement activation - Ensure C3b is densely deposited on microbial surfaces; not on the surfaces of human cells - Plasma protein = properdin (Factor P) - Factor P binds to C3 convertase (C3bBb) on microbial surfaces and protects it from inhibition by factor H - Factor H plasma protein reduces complement reactions by making C3b susceptible to cleavage by factor I creating a iC3b fragment that is incapable of forming a C3 convertase - On human cells the complement pathway is stopped by human cellsurface proteins decay-accelerating factor (DAF) and membrane cofactor protein (MCP). - DAF and MCP control proteins destroy C3 convertase activity by binding to C3b and displaces Bb and/or renders C3b susceptible to cleaved by factor I

qq. What protein/s degrades complement fragments and convertases? - Decay-accelerating factor (DAF) and Membrane cofactor protein (MCP) - DAF and MCP control proteins destroy C3 convertase activity by binding to C3b and displaces Bb and/or renders C3b susceptible to cleaved by factor I rr. Can we still recognize complement fragments on a pathogen if they have been cut by Factor H and factor I? By what receptors? - Yes - CR1 recognizes C3b - CR1 can also play a protective role by C3 susceptible to factor I  iC3b - CR2 is a B-cell co-receptor and recognizes C3d - CR3 & CR4 recognize iC3b - iC3b can be recognized by phagocytic cells ss. What are the acute phase proteins? How do these interact with complement? What is an example of an Acute phase protein as mentioned in class? - Acute-phase response increases the supply of the recognition molecules of innate immunity - Shows opsonization of pathogen by MBL and CRP tt. What are Defensins and what do they do? - Amphipathic (both hydrophobic and hydrophilic) - Penetrates the microbial membranes and disrupts - There are two types of defenses - α- defensins - Produced mainly by neutrophils and Panteth cells (specialized epithelial cells of the small intestine) - β- defensins – Expressed mainly by epithelial cells of the respiratory tract the urogenital tract and the skin

C1q can bind to multiple things like 2 IgG or 1IgM or 1 CRP all complement pathways could potentially lead to direct pathogen destruction through MAC. But, for classical and lectin, these two pathways are similar. The only difference between those two is how they are initiated. MBL is for lectin activation MASP2 cleaves C4 into C4a and C4b, C4b binds the surface of the pathogen. Then MASP2 cleaves C2 into C2a and C2b, C2a binds to C4b to form C4b2a (C3 convertase of the classical pathway)...