Fundamentals I Test 4 Barnum – Flashcards
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| What portion of the Immune System is important in adaptive immunity and is where T-cells are formed & mature? |
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| Thymus |
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| What portion of the immune system houses most of the immune cells that deal with blood born infections? |
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| Spleen |
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| What portion of the Immune system consists of small collections of lymphoid tissue that help clear local infection? |
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| Lymph Nodes |
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| What types of cells are important for adaptive immunity? |
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| T & B cells |
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| What types of cells are important in Innate Immunity? |
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| Macrophages, neutrophils, dendritic cells |
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| Name the Antigen presenting immune cells. |
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| Dendritic Cells, B cells, and Macrophages |
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| What types of cells are important in allergic responses? |
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| Mast Cells |
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| Describe the Innate immune response. |
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| first line of defense, works with adaptive (may be able to clear infection w/o adaptive), almost immediate response, less divers |
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| Describe the Adaptive immune response. |
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| takes time b/c specific T & B cells must be found & replicated, more specific, more likely to cause auto-immune problems |
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| Name the organs of the body that work via Innate Immunity to protect the host. |
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| Skin, Mouth & upper alimentary canal, Stomach, Small Intestine, Large Intestine, Airway & Lungs |
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| Describe the process of Phagocytosis. |
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| Bacteria attaches to membrane, ingested formong a phagosome, phagosome fuses to lysosome, enzymes digest material, digestion products released |
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| Describe the process of Inflammation. |
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| Tissue damage triggers vasoactive & chemotactic factors that cause increase blood flow & capillary permeability, fluid & cells exudate from capillaires, phagocytes migrate to site via chemotaxis, phagocytes & exudates destroy bacteria |
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| What structures help the innate immune system recognize infection? |
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| Pathogen Associated Molecular Patterns (PAMPs) |
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| What are the receptors for microbial components such as LPS, lipoproteins, peptidoglycan & ssRNA? |
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| Pattern Recognitation Receptors (PRRs), ie. Collectins, CRP, & Toll-like |
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| What type of receptors use an extracellular receptor to interact w/intracellular component to trigger cytokines? How does its recognition work? |
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| Toll-like Receptors (TLRs); it recognizes classes of bacteria not individual bacteria |
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| What is described as encountering pathogen getting sick then being immune or getting vaccine to get immunity? |
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| Active Immunity |
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| What is being immune w/o encountering pathogen ie. given Abs? |
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| Passive Immunity |
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| What has B cells that have been triggered to become Plasma cells? |
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| Humoral Immunity |
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| What's the most important cell in Cell-mediated Immunity? |
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| T-cells |
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| What type of immune cells prodcue cytokines that direct the immune response? |
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| T helper Cells |
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| What type of immune cells are turned on by Th1 cells and directly kill body cells that have been invaded by virus or bacteria inducing apoptosis? |
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| T cytotoxic Cells |
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| What is described as T regulatory cells ; cytokines helping turn T cell response back off after infection? |
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| Self-Limiting Response |
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| What helps combat self-reactive T cells? |
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| Tolerance |
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| What are the two most important functions of cytokines? |
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| regulate immune system and therapeutic reagents |
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| What is the term for cytokines made by monocytes? What about those made by activated T cells? |
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| Monokines; Lymphokines |
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| What cytokines are made by leukocytes ; act on leukocytes? |
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| Interleukins; now know lots of cells can make these |
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| What cytokines are important in controlling viral infections ; augmenting immune responses? |
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| Interferons |
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| What cytokines are important in the maturation of leukocytes? |
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| Colony-Stimulating Factors |
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| What cytokines are important in directed migration of leukocytes during immune responses? |
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| Chemokines |
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| What cytokines are involved in stem cell differentiation ; other functions? |
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| Growth Factors |
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| What are the four main functions of Cytokines? |
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1. Pleiotropic (mediate different fxns) 2. Redundant (can do the same thing) 3. Synergistic (when acting together their fxn is more than additive) 4. Antagonistic (help turn immune system off) |
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| Name 5 properties of cytokines. |
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1. low MW proteins or glycoproteins 2. Synthesized in active ; inactive forms 3. Secretion brief ; self-limiting 4. Active at very low concentrations 5. Signal cells by binding specific receptors on target cells |
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| What are the 4 main properties of cytokine receptors? |
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1. each cytokine has a receptor 2. grouped into 5 families 3. often mutli-chain complexes 4. signaling through receptors requires multiple events |
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| What are the 5 cytokine receptor families? |
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Immunoglobulin: IL-1 Class I: IL-2 (hematopoietin) Chemokine: IL-8 ; Chemokines Class II: IFN-;,;,; (interferon) TNF: TNF-;,; |
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| What portion of the cytokine receptor actually binds to the cytokine?; Which portion send signals to direct cell activity? |
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Cognate receptor subunit; Signaling receptor subunit ; |
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| How can cytokine receptors send signals to effect transcription? |
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| JAK's phosphorylate STATs which dimerize & can cross the nuclear membrane in order to effect transcription |
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| What effect occurs when a cytokine acts on the cell that produced it? Give an example. |
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| Autocrine; IL-2 → Tcells |
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| What effect is described as a cytokine acting on adjacent/nearby cells? Give an example. |
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| Paracrine; Interferons |
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| What effect is described as a cytokine acting on distant parts of the body like a hormone? Give an example. |
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| Endocrine; TNF & IL-1 |
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| What cytokine is an important signal for B cells to continue maturation? |
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| IL-7 |
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| What cytokine are T cells dependent on for activation after Ag binding? |
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| IL-2 |
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| What is aided by cytokines produced by Th1 cells? Give examples of these cytokines. |
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| Cell-mediated Immunity; IFN-γ and IL-2 |
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| What is aided by cytokines produced by Th2 cells? Give examples of these cytokines. |
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| Antibody production; IL-4,5,6 |
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| What cytokine is a major growth factor for B cells? What cytokines are involved in isotype switching? |
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| Growth factor=IL-6; Isotype switching= TGF-β for IgA and IL-4 for IgE |
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| What recognized viral genetic material as foreign? What does their binding lead to? |
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| TLRs; production of Interferons |
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| What are the two types of interferons and where are they produced? What are their innate & adaptive functions? |
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Type I: produced by all cells (IFN-α/β) Type II: prodcued by active Tcells (IFN-γ) Innate: viral clearance Adaptive: lymphocyte activation/maturation, induces MHC expression |
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| What portion of the bacteria do TLRs bind? Give examples. |
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| PAMPS; TLR-4=LPS and TLR-5=flagellin |
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| What three events occur in Acute Phase Response? Which cytokines direct this response? |
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1. Eliminate invading pathogen 2. Prevent on-going tissue damage 3. Activte repair processes "Pro-inflammatory" cytokines: TNF-α, IL-1, IL-6, IL-8, and IFN-γ |
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| What are 6 characteristics of Tumor Necrosis Factor-Alpha? |
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| induced by LPS and made by fibroblasts & MO; activates myeloid cells; induce production of cytokines, initiates acute phase response (fever); induces adhesion molecule expression; toxic at high levels (septicemia) |
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| What are the three groups of Acute Phase Proteins? Give examples. |
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1. Host Defense Proteins: CRP, complement, fibrinogen 2. Proteinase Inhibitors: C1 inhibitor, α1-proteinase inhibitor 3. Anti-oxidants: Haptoglobin, ceruloplasmin |
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| What are chemokines classified by, what are they involved in, and where are they expressed? |
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| by Cysteine Motifs; inflammation, cell recruitment, lymphocyte trafficking, lymphoid organ development, & wound healing; in primary & secondary lymphoid organs |
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| What are the current cytokine therapies? |
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IFN-α: chronic myeloid leukemia, Bechet's disease, aggressive oral giant cell tumors TNF-;: root resorption, refractory posterior uveitis, rheumatoid arthritis, (anti) orofacial granulomatosis IFN-;: multiple sclerosis |
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| What is defined as a groupd of sequentially reacting protein, which upon activation, mediate a number of biological reactions important to host defense? |
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| Complement |
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| Tell whether the proteins of Activation, Regulation, and Receptors are Serum Soluble or Membrane Bound. |
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| Activation=Serum Soluble;; Regulation=Both;; Receptors=Membrane Bound |
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| What Domain do the following Complement Proteins belong to: Enzymes, Collectins, Cytolytic, Regulatory and Receptor, and True? |
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Enzymes: Serine Protease Domain Collectins: Collagen Stalk, Globular Domain, MACPF/CDC superfamily Regulatory and Receptor: SCR Domain "True" Complement Proteins: C3,4,5 |
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| T/F; The same fragments are generated through both the classical ; alternative pathways. |
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| True |
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| What are the functions of both cleavage products of C3 and C5? |
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C3a: Chemotaxis and Inflammation C3b: Opsonization, Neutralization, and Bcell activation C5a: Chemotaxis and Inflammation C5b: Lytic complex formation |
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| Describe the opsonization of C3b. |
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| covalently binds to surface of invading pathogen via amide (NH2) or ester |
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| What activates complement in each of the three pathways? |
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Classical: Ag-Ab complexes (uses one IgM or two IgG molecules) Mannan-Binding Protein: Mannose, N-acetylglucosamine Alternative: LPS, zymosan |
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| Describe the action of C1q. |
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| C1q auto-activates C1s ; C1r which activates the classical pathway |
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| Describe the make-up and function of C3 convertase. |
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| C2a + C4b (C2a=enzymatic portion); cleaves C3, when C3b is added to complex it becomes C5 convertase |
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| Describe the way in which the complement system causes a cell to lyse. |
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| C5b bind C6,7,8 which triggers C9 to form a pore to lyse the cell |
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| What initiates the alternative pathway?; Describe it's action. |
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| C3 tickover; C3 interacts with water which binds Factor B, Factor D cleaved Factor B leaving Factor Bb+C3H20 = Alternative Pathway Initiator Convertase (cleaves C3 & joins classical pathway) |
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| Describe the functions of C3a & C5a. |
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| Anaphylatoxic & Chemotactic molecules; Degranulation; Increased vascular permeability; Induce cytokine release, adhesion molecules, and acute phase protein expression; Induces respiratory burst |
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| What are the functions of C5b? |
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| Initiation of the Membrane Attack Complex leading to formation of membranolytic pore-forming complex and signals transduction for cellular events |
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| What are the functions of C3b? |
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| Opsonization of Ag-Ab complexes for clearance, Solubilization of immune complexes, and neutralization of invading pathogens |
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| What five things regulate complement? |
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1. Regulation proportional to amount of activator 2. Limited half-life of convertases 3. Inhibitory protein control early activation 4. Carboxypeptidases inactivate anaphylatoxins 5. Inhibitory proteins modulate MAC formation |
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| What is the effect of DAF on Complement? |
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| DAF binds C3b & prevents Factor B from binding to form C3 Convertase (Alt Path); if convertase is already formed, DAF can increase its decay |
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| What is the effect of CD59 on complement? |
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| binds C5b,6,7,8 complex & blocks C9 addition = can't form pore complex; if one C9 has already attached CD59 can prevent more from attaching ; the pore from growing |
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| Which complement deficiencies cause recurrent bacterial infections? |
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| Activation Component Deficiencies ; Terminal Component Deficiencies (common in Japan ; predisposed to Meningitis) |
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| What are the Complement Deficiencies that have to do with Regulatory Components?; What about those with Receptor deficiences? |
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| Reg=HANE(spontaneous inflammation, low C1 inhibitor levels), PNH (spontaneous RBC lysis), ; aHUS;; Receptor=SLE (also Activation - Lupus) |
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| At what level of the vasculature does leukocyte rolling take place? |
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| Post-Capillary Venules (b/c the vessels are smaller ; blood flow is slower) |
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| What are the four families of adhesion molecules? |
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1. Selectins: C-type lectins 2. Integrins: Heterodimeric Receptors, ;2-Integrins 3. Cell Adhesion Molecules (CAMs): made of Ig Domains 4. Signaling Molecules: chemoattractant ; chemokine receptors |
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| What are the physical factors influencing lymphocyte/leukocyte migration? |
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| Blood Flow, Physical Barriers, and Ability to Detect Infection |
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| What mediates rolling and where are these components found? |
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| Selectins ; Carbohydrate Ligans; P ; E-Selectins on endothelial cells, L-Selectins on leukocytes, ligands on both |
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| T/F; If you are missing even part of the sLe molecule the leukocytes will not stick. |
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| True |
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| What are the two ways to see leukocyte rolling? |
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| Intravital Microscopy and Parallel Plate Flow Chamber |
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| Which Immunoserveillance disorder results in no binding to selectins? |
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Incomplete Glycosylation of sLewx (LAD II is a Leukocyte Adhesion Deficiency) |
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| What does infection interacting with chemotactic receptors and ligands result in? |
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| Activates endothelial cells and lukocytes, causes "inside-out signaling", gradient-dependent migration of leukocytes |
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| What is the most common conformation of the ;2-integrins; what causes them to change conformation? |
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| closed/unactivated; expression of ICAM increases which results in inside-out signaling causing integrins to be in the open conformation and stick more tightly to the cell |
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| What type of integrin is expressed on neutorphils (PMNs) and Macrophages and is also called CR3 or CD18/CD11b? |
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| Mac-1 |
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| What is the result of missing functional CD18? |
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| CD18 is part of Mac-1; without it None of the CD's make it to the cell surface to be expressed, neither does CR4 (b/c CR4=CD18/CD11c) |
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| What molecules assist the leukocyte in diapedesis? |
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Proteases: open space b/w the endothelial cells PECAM: helps trafficking of cell into tissue, expressed on neutrophil & endothelial cell Mac-1 & ICAM: interact to help pull cell through JAM: Junction Adhesion Molecules, expressed on endothelial cells, interact with integrin molecules (act as train tracks) |
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| What molecule mediates rolling only in lymph nodes & why? |
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| PNAd; b/c you don't want lymphocytes sticking to the rest of your endothelium |
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| Where does Naive Lymphocyte Homing occur? |
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| High Endothelial Venules (found only in lymph nodes) |
