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BMS150 test 1 > Week 1 notes > Flashcards

Week 1 notes Flashcards

1
Q

innate immunity

A

1st line of defence, less specific, no memory, fixed response

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2
Q

adaptive immunity

A

specific, delayed response, T and B cells, has memory to increase specificity and speed
-diversity via genetic shuffling of receptors

-secondary immune response is faster and higher affinity

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3
Q

antigen

A

binds receptor of adaptive immune system

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4
Q

immunogen

A

a substance that can generate an adaptive immune response

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5
Q

epitope

A

molecule that binds a receptor; antigen has many epitopes

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6
Q

hapten

A

substance binds antibody but NO immune response “too small”

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7
Q

lymphocyte receptor repetoire

A

set of antigens in a given individuals immune system

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8
Q

clonal selection theory

A

-receptor on lymphocyte has unique specificity –> differentiated effector cells = clones of parent cell

-lymphocytes with receptors that bind self are destroyed = selected functional receptors

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9
Q

B cell receptor

A

-2 light and 2 heavy chains
-variable portions shuffled and bind antigen

-antibodies (secreted) bind protein antigens amino acid sequence: continuous or discontinuous

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10
Q

B cell vs T cell receptor

A

B cell: 2 light and 2 heavy chains

T cell receptor: 1 Alpha and 1 beta chain with variable and constant regions

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11
Q

T cell receptor

A

-1 alpha and 1 beta chain = variable and constant region
-antigen presentation: need antigen close by to bind: use MHC/HLA

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12
Q

autoimmune vs tolerance

A

autoimmune: immune response to self

tolerance: immunological unresponsiveness to self

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13
Q

immature vs naive

A

immature: cannot yet be activated

naive: mature cell that hasn’t been activated

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14
Q

activated or effector

A

cells active in immune response

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15
Q

anergic

A

cell that responds to receptor binding by deactivation of cell “go to sleep”

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16
Q

clone

A

group of effector T/ B cells that express same antigen receptor as parent cell

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17
Q

lymphoid cells

myeloid cells

A

lymphoid: T cells, B cells, NK cells, dendritic cells

myeloid: granulocytes (neutrophils, basophils, eosinophils, mast cells), monocytes (macrophages), dendritic cells

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18
Q

monocytes/ macrophages

A

monocyte in blood into macrophage in tissue via maturation

phagocytic, soluble messenger, present antigens to T cells

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19
Q

dendritic cells

A

resident in tissue, transport antigen to lymphoid organs, present antigens to T cells

20
Q

neutrophils

A

phagocytic, short lived (die in infected tissue= pus; purulent)

most numerous cell!

21
Q

eosinophils

A

parasites, hypersensitivity reaction

22
Q

basophils

A

Histamine, mucosa, hypersensitivity reaction, parasites

23
Q

mast cells

A

connective tissue, orchestrate hypersensitivity reaction, mucosal

24
Q

b cells vs T cells

A

B cells: bone marrow, activate –>plasma cell that secrete antibodies

T cells: thymus
CD4+ helper= activate other cells (macrophages, B cells)
CD8+ cytotoxic T cells- kill cells with foreign molecules

25
NK cells
innate immune system, lack specific antigen receptors, kill infected cells
26
lymphoid tissue
where lymphocytes interact with non lymphoid cells
27
primary (central) typhoid organs vs secondary (peripheral) lymphoid organs
primary: where lymphocytes are generated and mature (bone marrow and thymus) secondary: antigen + T/B cell receptor = adaptive immune -->lymph nodes, spleen, MALT, GALT
28
secondary (peripheral) lymphoid organs
lymph nodes: lymphatic vessels spleen: -red pulp: filter blood (RBCs) -white pulp: lymphocyte, B cells with lots of antibodies in corona and T cells in periarteriolar lymphoid sheet (PALS) MALT: gut, bronchioles;; collect antigen from mucos GALT: tonsils, adenoids, appendix, Peyers patch Peyers patch= T/B cell area, get antigens in epithelial surface of GI tract via M cells = trap dipper w B and T cells to kill antigen
29
innate immunity
has chemical, mechanical and microbiological barriers
30
chemical barriers of innate immunity
-lysozyme: in secretions; hydrolysis of peptidoglycan wall --> lyse cell wall of bacteria -antimicrobial peptide (AMPs)- defensives: kill gram negative and positive bacteria, secreted in mucos and stored in neutrophil granulesgr
31
phagocytosis
engulf and destroy via macrophages and neutrophils pro-monocyte (bone marrow)--> monocyte (blood) --> macrophage (tissue) = long lived neutrophils= short lived in blood, non dividing
32
phagocytosis
bind PRR on pseudopodia (PRRs bind opsonins, microbes or debris) --> phagosome (PI3 kinase) and ROS, pore forming AMPs, enzymes --> fuse with lysosome or neutrophil granules (and NADPH complex or nitric oxide --> kill bacteria
33
opsonin
secreted PRR that coats microbe (makes it a better target)
34
PRRs categories
1. pathogen associated molecular patterns PAMPs 2. danger associated molecular patterns DAMPs toll like receptors, nod like receptors, lectins (mannose receptor), complement receptor, FC receptors on antibodies
35
microbe killing via neutrophils
neutrophil granules with defensives (rich in cysteine): form pores --> lysis -cathepsin (protease) -cathelicidins (pore forming) -lysozyme (glycoside hydrolase) -lactoferrin (interfere with iron metabolism in microbes) -NET (neutrophil extracellular trap): :"stuck in trap"; surround bacteria and lyse via chromatin in DNA (histones are toxic to bacteria)
36
toll like receptors; what are their ligands
LPS, dsRNA, ssRNA, DNA, flagellin
37
Toll like receptors; what cytokines do they secrete what is the key adaptor
1. inflammatory cytokines (IL-1B, IL-6, CXCL8, IL-12, TNF alpha) 2.interferons: IFN alpha, beta and gamma --> autocrine and paracrine signals to activate macrophages and NK cells **MyD88 adaptor for TLR -if deficient: severe bacterial infections -if constitutively active: blood disorders and cancers
38
Nod like receptors
intracellular receptor in cytoplasm that get products of degraded phagocytose pathogens and DAMPs (with stress) -activate inflammatory cytokines
39
3 parts in acute in inflammation
1. vasodilate 2. increase vascular permeability 3. emigrate and activate leukocytes
40
acute inflammation;; vasodilate
increase blood flow then eventually lose fluid and slow blood flow= vascular congestion for margination of leukocytes -NO, histamine (via C3a, C5a), prostaglandins, platelet activating factor low [] NO = vasodilate high [] NO= destroy microbes and hosts membrane phospholipids--> phospholipase (PLA2) --> arachidonic acid --> cyclooxyrgenase (COX) --> prostaglandins (PGI2, PGD2, PGE2)
41
acute inflammation;; increase vascular permeability
via endothelial cell contraction or damage membrane phospholipids--> phospholipase (PLA2) --> arachidonic acid --> 5 lipooxygenase --> chemotaxis (leukotriene LTB4) -histamine, serotonin, prostaglandins, leuotreines, C3a, C5a, platelet activating factor, bradykinin increase transocytosis: vesicle mediated transport across capillary endothelial cell large molecules move across via pinocytosis and receptor mediated endocytosis lymphangitis: lymph vessel inflamed from interstitial fluid and microbe and leukocyte buildup
42
acute inflammation;; emigrate and activate leukocytes
neutrophils, basophils, eosinophils, monocytes a) margination: leukocytes migrate to vessel walls b) rolling: E and P selection-- form and dissociate adhesion bonds between leukocyte and endothelial cell = loose adhesion c) ahdesion: strong bond via chemokine and integral on leukocyte --> adhesion and rolling via selections and CAMs d) diapedesis/transmigration: leukocytes migrate through endothelium e) chemotaxis of leukocytes to site of injury or infection
43
cytokine vs chemokine
cytokine: protein messenger secreted chemokiens: small cytokines, bind leukocytes --> movement along [] gradient -adhesion for differentiation and migration -CXC; attract neutrophils -CC: attract other leukocytes
44
help leukocytes migrate to target
-histamine, thrombin: rolling, selection expression by epithelial cells -TNF and IL1: ICAM expression by endothelial cells -chemokines: increase integral affinity
45
chemotactic agents
leukocytes follow [] gradient to invasion site -leukotrien B4 -C5a -chemokines (IL8, eotaxin)
46
5 steps of emigration and activation of leukocytes in acute inflammation
1. margination 2. rolling (e and p selection) 3. adhesion (integrin and chemokine) 4. diapedesis/transmigration 5. chemotaxis of leukocytes to sites of injury or infection
47
complement
blood borne molecular defence system that complements antibodies helps with phagocytosis, destruction or microorganisms, inflammation activated via an enzyme cascade

BMS150 test 1 (1 decks)

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