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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
Q

NK cells

A

innate immune system, lack specific antigen receptors, kill infected cells

26
Q

lymphoid tissue

A

where lymphocytes interact with non lymphoid cells

27
Q

primary (central) typhoid organs vs secondary (peripheral) lymphoid organs

A

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
Q

secondary (peripheral) lymphoid organs

A

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
Q

innate immunity

A

has chemical, mechanical and microbiological barriers

30
Q

chemical barriers of innate immunity

A

-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
Q

phagocytosis

A

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
Q

phagocytosis

A

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
Q

opsonin

A

secreted PRR that coats microbe (makes it a better target)

34
Q

PRRs categories

A
  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
Q

microbe killing via neutrophils

A

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
Q

toll like receptors; what are their ligands

A

LPS, dsRNA, ssRNA, DNA, flagellin

37
Q

Toll like receptors; what cytokines do they secrete

what is the key adaptor

A
  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
Q

Nod like receptors

A

intracellular receptor in cytoplasm that get products of degraded phagocytose pathogens and DAMPs (with stress)
-activate inflammatory cytokines

39
Q

3 parts in acute in inflammation

A
  1. vasodilate
  2. increase vascular permeability
  3. emigrate and activate leukocytes
40
Q

acute inflammation;; vasodilate

A

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
Q

acute inflammation;; increase vascular permeability

A

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
Q

acute inflammation;; emigrate and activate leukocytes

A

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
Q

cytokine vs chemokine

A

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
Q

help leukocytes migrate to target

A

-histamine, thrombin: rolling, selection expression by epithelial cells

-TNF and IL1: ICAM expression by endothelial cells

-chemokines: increase integral affinity

45
Q

chemotactic agents

A

leukocytes follow [] gradient to invasion site

-leukotrien B4
-C5a
-chemokines (IL8, eotaxin)

46
Q

5 steps of emigration and activation of leukocytes in acute inflammation

A
  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
Q

complement

A

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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