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TERM 3- Premidterm > L15, L17- Innate Immune System > Flashcards

L15, L17- Innate Immune System Flashcards

1
Q

these two molecules (CKs) are responsible for repressing the immune system

A

IL-10

TNF-β

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2
Q

these three molecules (CKs) are responsible for inflammation response

A

IL-1
IL-6
TNF-α

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3
Q

these two molecules (CK) are responsible/signal of chronic inflammation

A

IFN-γ

IL-12

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4
Q

receptors and effectors of the innate immune system come from (1), there response is described as (2) and (3), while lacking (4)

A

1- germ-line DNA (fully defined)
2- rapid
3- invariant
4- memory

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5
Q

innate immune system has (1) receptors to recognize (2) and (3) patterns

A

1- Toll-like receptors
2- PAMPs (pathogen-associated molecular patterns)
3- DAMPs (damage-associated molecular patterns)

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6
Q

describe and provide a few examples of PAMPs

A

(pathogen-associated molecular patterns)
-recognized patterns are from essential parts of the microbe, involved in survival/matabolism and evolutionary stable

-exs: peptidoglycan, flagellin (flagella protein), LPS, dsRNA, mannose, non-Me CpG repeats

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7
Q

the key receptor of innate immune system is….

A

Toll-like receptors- recognizes PAMPs

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8
Q

toll-like receptors will have signal cascade to produce (1) and (2) to induce an antiviral state

A

1- INF α

2- INF β

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9
Q

after recognition by the innate immune system, pathogen will be marked for (1) via (2) or (3)

A

1- phagocytosis
2- monocytes//macrophages
3- neutrophils

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10
Q

list the general activities of phagocytes

A
  • survey tissue to discover microbes, particulate matter, dead/injured cells
  • ingest/eliminate those materials
  • extract immunogenic info from foreign matter (possibly APC)
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11
Q

Phagocytes use the addition of (1) as a marker to enhance phagocytosis. One example is the (2) receptor recognizing the (3) fragment in the complement cascade. Another is (4) receptors recognizing (5) region of Igs/Abs.

A

1- opsonin

2- CR1 receptors
3- C3b

4- Fc receptors
5- Fc

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12
Q

the main opsonin for Abs is (1), and there is not a Fc receptor for (2) which will activate (3) instead

A

1- IgG
2- IgM
3- complement

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13
Q

complement molecules opsonize antigens via (1) receptors on phagocytes, where these three are the main opsonins: (2)

A

1- CR1 receptor

2- C3b, C4b, C1q

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14
Q

besides Abs/Igs and complement molecules, these are the other opsonins

A

circulating proteins (secreted pattern recognition receptors): pentraxins, ficolins, collectins (mannose-binding lectin / MBL)

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15
Q

describe the step of phagocytosis

A

1) chemotaxis / ingestion: migration to and recognition of PAMPs => initiation and perpetuation of inflammatory response
2) phagolysosome formation: lysosome fuses with phagosome => death ~30 mins
3) destruction/elimination: via O2 dependent system / respiratory burst + liberation of lactic acid, lysozyme, NO

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16
Q

list the oxygen independent mechanisms of phagocytic killing (hint: there are 4)

A
  • lysozyme: split peptidoglycan
  • lactoferrin & reactive nitrogen intermediates: deprive pathogen of Fe
  • proteolytic enzymes: degrade dead microbe
  • defensins, cathepsin G, cationic proteins: damages microbial membrane
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17
Q

(1) stimulates macrophages to produce NO, which is then released to (2), this is important for (3) situations

A

1- INF-γ
2- kill nearby microbes
3- microbes/organisms that escape oxidative burst

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18
Q

the most important enzyme for oxygen-dependent phagocytosis is _______ [include rxn]

A

NADPH oxidase: O2 –> *O2- (superoxide ion)

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19
Q

after function of NADPH is complete, these following reactions occur….

A

1st: *O2- (superoxide anion) –> H2O2 via Superoxide Dismutase
2nd: H2O2 + Cl- –> HClO- (hypocholorite) via Myeloperoxidase

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20
Q

CGD, aka (1), is the result of (2) and results in (3)

A

1- chronic granulomatous disease
2- lack of NADPH oxidase (genetically)
3- recurrent infections (ex: pneumonia, abscesses, arthritis, osteomyelitis, bacteremia/fungemia, cellulitis, etc)

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21
Q

describe the test for CGD

A

(chronic granulomatous disease)

  • Nitroblue-tetrazolium (NBT) test
  • if NADPH oxidase present –> NBT is reduced and turns blue
  • if absent –> negative yellow color persists
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22
Q

CHS, aka (1), is a (2) inherited disorder resulting from (3). This disease is characterized by (4) being present in phagocytes. Clinical presentation is (5).

A

1- Chediak-Higashi Syndrome
2- autosomal recessive
3- mutation of lysosomal trafficking regulatory protein (=> no lysosomal-phagosomal fusion)
4- large lysosomal vesicles
5- albinism (silver hair), neutropenia, periodontal disease, recurrent infections

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23
Q

list the signs and symptoms of inflammation (hint: 5)

A
  • rubor (redness)
  • calor (hot/warm)
  • tumor (swelling)
  • dolor (pain)
  • loss of function
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24
Q

in the first step of inflammatory response, injury causes (1) leading to (2)

A

(injury/immediate reactions)
1- release of chemical mediators, CKs, histamine
2- attraction of leukocytes to site of injury

Note- brief vasoconstriction occurs

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25
Q

in the second step of inflammatory response, (1) causes (2) leading to redness and warmth and functions to enhance delivery of the following to the site of injury: (3)

A

(vascular reactions)
1- Histamine
2- vasodilation
3- leukocytes, fluid, clotting factors

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26
Q

in the third step of inflammatory response, (1) helps contain the infection and attract (2) which collects debris to form (3); also, (4) is present to stimulate pain receptors

A 
(edema/pus formation)
1- edema
2- neutrophils
3- pus
4- bradykinin
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27
Q

in the fourth (and final) step of inflammatory response, (1) clean the area, (2) forms granulation tissue, and (3) come to mediate long-term immunity

A

(resolution/scar formation)
1- macrophages
2- fibroblasts
3- lymphocytes

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28
Q

_______ is the migration of cells out of blood vessels into the tissues

A

diapedesis

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29
Q

______ is migration in response to specific chemical at site of injury/infections

A

chemotaxis

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30
Q

list the four types of CAMs

A

(cell adhesion molecules)

  • selectins
  • mucins
  • integrins
  • ICAMs (Ig CAMs)
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31
Q

ICAMs/Ig CAMs are expressed on (1) cells and bind to (2)

A

1- endothelial cells

2- integrins (on leukocytes)

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32
Q

Integrins are described as (1) in structure and are only expressed on (2) cells and bind to (3)

A

1- proteins, heterodimers
2- leukocytes
3- Ig superfamily molecules

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33
Q

Mucins are described as (1) in structure and are found on (2) and (3) cells; functioning to present (4) to (5)

A 
1- proteins
2- endothelial cells
3- neutrophils
4- CHO ligands
5- selectins
34
Q

Selectins are described as (1) in structure and are found on (2) and (3) cells and bind to (4)

A

1- glycoproteins
2- leukocytes
3- endothelial cells
4- carbohydrates

35
Q

describe the four steps to leukocyte extravasation (of neutrophils and monocytes)

A

1) rolling: via selectins (endothelium) to mucins (leukocytes)
2) activation: chemokine binding => conformational change in integrins (leukocytes)
3) arrest/activation: integrins bind Ig CAMs (endothelium)
4) transendothelial migration: leukocytes through tight junctions of inflamed endothelium

36
Q

LAD, aka (1), is an inherited deficiency in (2) which usually dimerizes with (3) and binds (4) receptors, therefore neutrophils cannot migrate through endothelium

A

1- leukocyte adhesion defect
2- β-2 integrin subunit (CD18)
3- CD11 subunits
4- ICAM-1

Note- no pus formation, high levels of neutrophils in blood

37
Q

Hagman factor (XII) activation leads to activation of (1) causing (2) + (3) formation to stop (4) and eventually (5) to reverse (3) and activate (6)

A

1- bradykinin formation
2- vasodilation, permeability, pain, smooth muscle contraction

3- thrombin/clot formation
4- stop bleeding
5- plasmin (breakdown clots)
6- activates complement

38
Q

the complement system as a mediator to inflammation uses (1) to activate (2) cells and increase (3) in the site of injury/inflammation

A

1- anaphylatoxins
2- mast cells
3- increase permeability

39
Q

the following chemical mediators are responsible for the chemotaxis / infiltration of neutrophils in the inflammatory process

A

IL-8
LT-B4
C5a
fibrinopeptides (acting as chemokines)

40
Q

these three chemical mediators released from activated tissue macrophages, (1), will act on (2) to induce fever, (3) to increase acute phase proteins, and (4) for increased leukocytosis

A

1- IL-1, IL-6, TNF-α
2- hypothalamus
3- liver
4- bone marrow

41
Q

the main acute phase protein resulting from inflammatory process is (1) and acts to (2)

A

1- C-reactive protein

2- activate complement

42
Q

increased leukocytosis is also known as…..

A

Left shift (inc immature/band cells)

43
Q

chronic inflammation is defined as (1) and is mainly mediated by (2) and (3)

A

1- inflammation > 2 wks (failed acute inflammatory response)

2- IFN-γ, TNF-α

44
Q

the main anti-inflammatory drugs are….

A
  • corticosteroids

- NSAIDs

45
Q

these two molecules are the main two chemokines signalling for neutrophil migration

A

IL-8

C5a

46
Q

list the groups of soluble proteins of the innate immune system

A
  • antimicrobial serum agents
  • proteins produced by cells
  • Complement system: series of proenzymes
47
Q

______ is a Fe binding protein that competes with microbes for Fe (an essential metabolite)

A

lactoferrin

48
Q

CRP is an acute-phase protein that binds to (1) on bacterial membranes and functions as an (2) and to activate complement via the (3) pathway.

A

(C-reactive protein)
1- phosphocholine
2- opsonin
3- classic pathway

49
Q

(1) recognizes carbohydrate patterns found on various microbes to activate the (2) pathway of the complement system

A

1- MBL (mannose-binding lectin)

2- lectin pathway

50
Q

(1) recognizes LPS on bacterial cell walls and serves as a receptor for (2). It is also implicated in several (3) diseases.

A

1- SAP (serum amyloid A protein)
2- phagocyte attachement
3- chronic inflammatory diseases

51
Q

list some antimicrobial serum agents

A
  • lactoferrin
  • CRP (C-reactive protein)
  • MBL (mannose-binding lectin)
  • SAP (serum amyloid A protein)
52
Q

INF-α/β are small proteins produced by (1) and (2) in response to (3) to work on (4) cells via (5) mechanism.

A

1- WBCs
2- virally infected cells (any cell type)
3- virus, RNA, immune products, various antigens
4- neighboring cells (unaffected)
5- inhibit transcription / translation of viral proteins

53
Q

INF-α/β are considered INF type (1/2).

A

type 1

54
Q

INF-γ is considered INF type (1/2).

A

type 2

55
Q

INF-γ is produced by (1) cells and list some of its functions: (2)

A

1- Th1, CTLs (CD8+), NK cells
2- promote NK activity, inc macrophage activity, inducible NO synthase (vasodilation, SM relaxation), induce Ig production, inc MHC I/II on normal cells, promote leukocyte adhesion/migration, induce antiviral defense mechanisms. responds to cancerous growth

56
Q

INF-γ is heavily involved in (1) formation as the body cannot remove such a substance- describe mechanism of (1): (2)

A

1- granuloma formation
2- macrophages activate Th1 via IL-1, IL-12 –> Th1 cells aggregate around macrophages –> INF-γ is released to activate macrophages –> repeat until macrophages wall off infection

57
Q

Complement makes up (1)% of serum globulin, with >20 serum glycoproteins synthesized by (2). These complement proteins circulate as (3) and are activated by (4)

A

1- 5%
2- mainly hepatocytes + monocytes, macrophages, epithelial cells
3- proenzymes (inactive)
4- cleavage => cascade reaction

58
Q

complement system is generally important to (1) and (2)

A

1- recruitment of inflammatory cells

3- killing/opsonization of pathogens

59
Q

what are the three inactive precursors of complement in blood

A

C2, C3, C4

60
Q

list the complement pathways

A
  • Classic: Ab-antigen
  • Alternative: microbial or non-microbial foreign substances
  • Lectin: MBL
61
Q

all complement pathways lead to the production of (1) opsonin, recognized by (2) receptor

A

1- C3b

2- CR1

62
Q

list the three inflammation inducing complement proteins

A

C3a, C4a, C5a

63
Q

Classical Complement Pathway is apart of (innate/adaptive) system with the following steps: (2)

A

1- adaptive
2- C1 binds Ag-Ab complex –> activated C1 cleaves C4/C2 –> C3 convertase formation –> C3 cleaved (C3a, C3b) –> C5 (a/b) cleaved –> sequential binding of C5b, C6-C9 + inflammation (C5a) –> MAC formation (hole in pathogen membrane –> cell lysis)

64
Q

Alternative Complement Pathway is apart of (innate/adaptive) system with the following steps: (2)

A

1- innate
2- spontaneous C3 cleavage (into a/b) via multiple initiators –> factors B/D required –> less stable C3 convertase formed (requires properdin) –> opsonization + inflammation

65
Q

MBL Complement Pathway is apart of (innate/adaptive) system with the following steps: (2)

A

1- innate
2- MBL + acute phase protein (serum) binds carb residue on cell/pathogen –> MBL-associated serine protease binds MBL –> C2/C4 into C2a/b + C4a/b –> C2a/C4b activate C3 –> C3b (opsonization, cytolysis) + C3a (inflammation)

66
Q

all three complement pathways converge with activation of (1) where the product (2) binds to antigenic surface leading to (3) formation by the following components: (4)

A

1- C5 convertase
2- C5b
3- MAC
4- C5b, C6, C7, C8, C9 (Poly-C9 => perforin-like molecule)

67
Q

list the functions of complement (hint- 5) and their associated molecules

A
  • Cell lysis, C5b-C9 (Ab dep. or indep.)
  • Opsonization (C3b)
  • Inflammation (C3a, C5a)
  • Clearance of Immune complexes (C3b)
  • Viral neutralization (C3b, C5b-C9)
68
Q

anaphylatoxins include….

A

C3a, C5a

69
Q

list the three targets of complement inhibitors and include some examples

A

1) C1 inhibitor (classical)
2) MAC formation: CD59, clusterin, protein S (all pathways)
3) C3 or C5 convertase (all pathways)

70
Q

what are the MAC formation inhibitors (hint- 3)

A

CD59
clusterin
protein S

71
Q

list the two types of complement deficiencies

A
  • Activator disorder => under-reactive system => more susceptible to infections
  • Inhibitor disorder => over-reactive system
72
Q

classical pathway component deficiencies include loss of (1) molecules leading to individuals prone to immune complex disease with (2) and (3) characteristics; examples include: (4)

A

1- C1, C2, C4
2- inability to clear circulating immune complexes
3- deposition in tissues and associated inflammatory response
4- lupus (SLE), vasculitis, glomerularnephritis

73
Q

MBL deficiency leads to (1) presentation and susceptibility to (2) infections

A

1- recurrent pyogenic infections in childhood (via Staph.)

2- Saccaromyces cerevisiae, pneumococcal, Neisseria infections

74
Q

alternative pathway components that can be lost include (1) molecules and leave individuals prone to (2)

A

1- properdin, factor B, factor D

2- pneumoccocal, meningococcal infections + Neisseria infections (if properdin)

75
Q

C3 deficiency is critical as C3 is necessary for (1) and presentation is as follows: (2)

A

1- opsonization

2- early in life with many infections via encapsulated organisms (more in CTs)

76
Q

MAC deficiencies is a lack of one of the following components: (1), and (2) as its presentation

A

1- C5-C9

2- recurrent infections (commonly Neisseria meningitidis)

77
Q

loss of C1-INH, which regulates (1) pathway, results into (2) via (3) accumulation

A

1- classical pathway
2- angioedema
3- C2b accumulation (vasoactive substance)

78
Q

DAF, aka (1), and (2) are responsible for (3) and its deficiency leads to (4)

A

1- decay accelerating factor, CD55
2- CD59
3- dissociation of C3 convertase
4- Paroxysmal Nocturnal Hemoglobinuria (lysis of RBCs)

79
Q

most complement diseases are inheirted via (1) or acquired via (2); note (3) and (4) are also possible

A

1- autosomal recessive
2- acquired post-infection
3- X-linked (properdin deficiency)
4- AD (MBL deficiency can be AD or AR)

80
Q

hereditary angioedema is characterized by the Sxs (and absence of a Sx)

A

-episodic, nonpruritic localized SQ/submucosal swelling
[-laryngeal edema can => fatal respiratory obstruction]
-absence of urticaria/rush (distinguishes it from allergic reaction)

81
Q

list the mechanism of hereditary angioedema

A

Dysregulation of 3 systems:

  • Complement (classical): no C1-INH => high [C3a, C5a] (anaphylatoxins) => inflammation
  • Coagulation- factor XI/XII => fibrin build-up => Edema
  • Contact cascade- inc Bradykinin levels => pain, inflammation, coagulation
82
Q

would a C1-INH defect result in elevated or decreased C4

A

decreased C4

TERM 3- Premidterm (20 decks)

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