Exam 3 Study Guide
Exam 3 Study Guide 4000
Popular in Basic and Practical Microbiology
Popular in Microbiology
This 6 page Study Guide was uploaded by an elite notetaker on Tuesday November 10, 2015. The Study Guide belongs to 4000 at Ohio State University taught by Madhura Pradhan in Fall 2015. Since its upload, it has received 109 views. For similar materials see Basic and Practical Microbiology in Microbiology at Ohio State University.
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Date Created: 11/10/15
Exam 3: Innate and Adaptive Immunity Innate Immunity Chapter 14 Pattern Recognition Receptors (PRRs) slide 16/35 PRRs detect pathogenassociated molecular patterns (PAMPs), by seeing signs of microbial invasion expressed on the surface of our cells examples of PAMP: LPS, peptidoglycan, teichoic acid, lipoproteins, flageliin subunits, viral RNA molecules o Tolllike receptors (TLRs) one type found anchored in the membranes of sentinel cells, anchored in WBCs; able to recognize pathogens outside our own cells; also able to recognize pathogens within the cell (b/c of phagocytosis) 1. Extracellular environment (so it can recognize pathogens circulating outside the cell) 2. Lined with a membrane o Nodlike receptors (NLRs) not anchored in the membrane but instead in the cytoplasm can only recognize pathogens INSIDE the cell (cytoplasmic/intracellular) o Riglike receptors (RLRs) found in the cytoplasm too (so only recognize intracellular) difference between NLRs: RLRs recognize viral infections what happens after the pathogen is recognized?: take action against the pathogen but also then send signal to the rest of your body Cell Communication 1. Surface receptors: “eyes” and “ears” of the cell (aka PRRs) 2. Cytokines: “voices of the cell” sends signal to the rest of your body produced by cell diffuse to others bind to appropriate cytokine receptors to induce changes such as growth, differentiation, movement and cell death act at low concentration; effects local, regional, systemic can be used to reduce 3. Types of cytokines MOST IMPORTANT a. Chemokines: allows movement of WBCs (promotes chemotaxis), to get to where the infection is occurring b. Colonystimulating factors (CSFs): required for multiplication and differentiation of WBCs (leukocytes); gives signal that they need to increase number because of infection c. Interferons (IFNs): be prepared because there is a specific virus infecting a cell, regulation of inflammatory response; will protect other cells in that tissue against the virus d. Interleukins (ILs): produced by WBCs (leukocytes); role in both innate and adaptive immunity; maintains balance with the proper type of interleukins DETECTION OF PATHOGEN HAS NOW ENDED NOW WE MOVE TO DESTRUCTION: PART II Second Line defenses: 1. Detection 2. Destruction of pathogens: phagocytosis, etc Be able to describe the big picture and then move on to fill in the details A. Phagocytosis phagocytes engulf and digest pathogens; not only damaged cells but also the damaged cells and debris left behind 1. Chemotaxis: what attracts them: products of microorganisms, chemicals from our own injured cells Neutrophil: phagocytic (professional) Basophil: not phagocytic Eosonphil: small extent phagocytes Macrophages: phagocytic (professional) Lymphocytes are absolutely NOT phagocytic and do not play a role in innate immunity 2. Recognition and attachment: key step because there has to be physical contact Attachment: can be direct (receptors bind bacteria) or indirect (binds to opsonins on bacteria) opsonins: when present it is much easier to exocytose 3. Engulfment: 4. Phagolysosome formation: lysosome needs to bring the digestive enzymes to destroy what is in the phagocyte 5. Destruction and digestion 6. Exocytosis neutrophils: first cells to arrive at the point of inflammation The Inflammatory Response Cause of inflammation: Either infection or mechanical damage tissue damage resulting in inflammation protective response to the infected tissue can occur even without infection i.e. mechanical damage Signs and symptoms (they are different!!) swelling redness: because of increased blood flow to the inflamed area pain: due to release of certain chemicals or others heat Must have these 4 to be considered inflammation sometimes loss of function: not always present during inflammation Triggers for inflammation chemicals: cytokines, histamine and bradykinin = secreted within our own tissue The Inflammatory Process 1. Vasodilation: 2. Migration of leukocytes from bloodstream to tissues via exravasation: neutrophils are first responders diapedesis: squeezing between blood vessels and coming out 3. Phagocytosis (destruction of invaders) Neutrophils first, then clotting factors: in liquid part of the blood macrophages Short term: acute inflammation, chronic works if acute fails Damages of Inflammation The Complement System Proteins in blood and lymph “bathing” tissues: kept inactive because we don’t want them attacking our own cells; activated when there is an infection Just know that theres 3 C1C9; can fragment ex. C3 C3a and C3b Activated by 3 pathways: alternative, lectin, classical; all by presence of pathogen in our body One more requirement for classical activation: there must be the presence of an antibody Functions of complement proteins: 1. Opsonization: entire surface of a pathogen is coated by an opsonin (ex opsonin: complement protein C3b) 2. Inflammatory response: C3a and C5a 3. Membrane attack complexes: on surface of pathogen(bacterial)membrane leads to lysis of foreign cells Interferon production not pathogen specific production is stimulated by infection Chapter 15: Adaptive Immunity lymphocytes: responsible for adaptive immune response Two Branches: 1. Humoral: free circulating in our body produce pathogens 1. Blymphocytes (B cells) 2. Cellmediated Immunity: 3. BCR of B cell 4. Plasma cells: physically secreting antibodies, hundreds every second; will have the same specificity 5. Antibodies with high levels of specificity Cellmediated immunity: 1. Tlymphocytes: mature in the thymus (how they get their name) a. Subsets: most commonly discussed i. Cytotoxic Tcells ii. Helper T cells iii. Regulatory Tcells: don’t recognize antigens but prevent immune system from mounting a response against our own tissues b. Antigens can only be recognized by Tlymphocytes IF they are presented on the cell’s OWN body Primary lymphoid organs: only bone and thymus lymphocytes cycle through organs and blood and will only stay in the secondary organs if they encounter secondary lymphoid organs o Secondary lymphoid organs: Ex. a. Lymph nodes: located throughout our body where immune response is produced b. Spleen: bloodborne pathogens c. Tonsils, adenoids, appendix d. SALT(skin associated lymphoidic tissue) e. MALT(mucus associated lymphoidic tissue) ex. Peyers patch: under mucus membranes all places active immune responses are produced Wednesday 4 th Tdependent Humoral Response – not very common, independent more common 1. Bcell receptor recognizes antigen internalization of antigen (B lymphocytes ARE NOT PHAGOCYTIC) they use ENDOCYTOSIS 2. Fragments are expressed on the surface of the B cell ONLY if they are combined with MHC class II molecules 3. Thelper cells inspect antigen fragments a. BLymphocytes will NOT go further unless they receive a signal from Thelper cells initiating clonal expansion b. If no Thelper cells: B cell becomes unresponsive tolerance to antigen then continues to normal humoral response will only occur after receiving cytokines ******PLASMA cells can never recognize antigens, their only job is to secrete antibodies*** adaptive immunity improves over time: happens in Tdependent responses o Primary Humoral Response: produce antibodies against the pathogen for the very first time 1. 1014 days to accumulate antibodies 2. IgM: ALWAYS the first class of antibody to be produced: quantity and quality of antibody is low the first time in primary response 3. the person may be sick but the immune system can be actively responding 4. additional exposure to the antigen will lead to a much faster secondary response **these last steps are what make the secondary response stronger**: o Affinity maturation: improve the quality of the antibody produced in humoral response mutations in the Blymphocytes change the affinity, the lymphocytes with the higher affinity to the antigen will be the ones to survive as they multiply they have a better Bcell receptor “memory cells” o Class switching: to change the class of antibody secreted plasma cells normally secrete IgM but Thelper cells can activate B cells to secrete other antibody classes: Lymph nodes: IgG MALT: IgA secondary responses are always much better than primary responses o Secondary Humoral Response: 1. Significantly faster and more effective then primary response (the idea behind vaccinations) Nature of Antibodies proteins made of protein chains 1. Antibodies (Ab) aka immunoglobulins (Ig) 2. yshaped proteins: Two regions: a. Arms: Fab region b. Stem: Fc region light chain (2): only in arms heavy chains (2) bonded by disulfide Variable region (2 for each type of chain): at the tip, (blue on heavy chain, green for light) ** the attachment site of antigens The rest of light chain just provides shape Fc region: serves as classification as type of antibodies changes 11/9/15 Function of Antibodies 1. Neutralization: strategically bind to pathogens (toxins and viruses) so that they can no longer bind to their host cell 2. Opsonization: easily captured by phagocytic cells because they have receptors for the bacterium, antibodies serve as opsonins (other opsonins: C3b) 3. Complement system activation: membrane attack complex formation which leads to lysis of bacterium (antibodies themselves are not directly killing the pathogen, but assist other mechanisms) 4. Immobilization and prevention of adherence 5. Aggregation: antibodies can bind 2 bacterium, therefore they form “crosslinks”: agglutination IgM: is the most effective because it has 10 arms and can therefore bind 10 antigens 6. ADCC (antibodydependent cellular cytotoxicity): 5 major classes of Antibodies: (interchangeable with immunoglobulin) 1. IgM 2. IgG 3. IgA 4. IgD 5. IgE must know distinct functions and properties of each class all information in the slides Tcells Tcell receptor and CD coreceptor work together to function, one cannot work without the other *****CD4 is the receptor for HIV Antigen recognition: antigen + MHC complex is recognized by Tcell receptor and CD coreceptors MHC molecules: 1. Class 1 MHC: every nucleated cell has these allows our immune system to recognize self v. nonself (everyone’s class 1 is different) ex. Rejection of tissue that is not our own endogenous antigens o In combination with different proteins, different things will happen (listen to recording ~22 min) 2. Class II exogenous antigens (not an infection) – captured outside, degraded inside : CD4+ TCR Antigen recognition by Tcells (*********very important slide) CD8+= MHC class 1 CD4+= MHC class 2 o Cytotoxic T cells (cells): MHC class I ~23 min o Helper T cells: MHC class II production of memory cells as well T secrete H: macrophages: become activated after receiving cytokines from T Hcells
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