Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MCM Quiz2 > Innate Immunity:Early Defense Against Infections > Flashcards

Innate Immunity:Early Defense Against Infections Flashcards

1
Q

what are the 4 cardinal signs of inflammation?

A

tumor (swelling) rubor (redness) calor (heat) dolor (pain), functio laesa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what cells cause inflammation to happen?

A

Mast cells!: histamine, prostaglandins,leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do mast cells do as POTENT VASODILATORS?

A

cause contraction of nonvascular smooth muscle, increased vascular permeability, and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mast cells Macrophages Dendritic cells, what are they, what do they do?

A

sentinel cells that respond to microbes

Secrete inflammatory mediators,

Increased vasvular permeability, proteins enter tissues,

Complement and antibodies kill microbes,

Cytokine cause leukocute migration to tissue,
Killing of microbes through phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what do LEUKOCYTES do?

A

attack the invading microorganisms and release substances (mediators) that continue the process of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

BODY REACTIONS to the substances released during inflammation ?

A

chills, fever, and muscle aches that commonly accompany infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Innate responses, can they prevent infection?

A

often sufficient to prevent infection within tissues or the blood. However, inflammation may not be able to overcome large numbers of microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is fever caused by?

A

not directly caused by pathogenic factors. Rather, bacterial constituents trigger production of the pyrogenic cytokines TNF, IL-1, and IL-6 in Mf which are potent inducers of fever response controlled by the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the first functional barrier for microbes?

A

The SKIN and MUCOUS MEMBRANES

have ANTIMICROBIAL SUBSTANCES and are covered by CILIA, which function to trap organisms in mucus and propel them out of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does sebum inhibit microbes?

A

fectively reduce skin pH to between 3 and 5 to inhibit growth of microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mucous membranes ,TEARS, SALIVA, and NASAL & BRONCHIAL TISSUES?

A

contain iGa, stop microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Innate immunity has the ability to discriminate between self and nonself how?

A

uses PAMPs

PAMPs are unique to particular classes of pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

whats so special about PAMPs?

A

cannot be altered, suppressed, or hidden from the surface by pathogens

no structural similarity with self Ags

ex:1. Porins 2. Lipoproteins 3. Lipopolysaccharides 4. Lipoteichoic acid 5. Teichoic acid 6. Mannoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are damps?

A

DANGER MOLECULES that are released from
damaged or dying cells.

induce potent inflammatory responses by activating the innate
immune system during NON-INFECTIOUS INFLAMMATION

recognized by Mf via TLRs which trigger an
inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is necrosis?

A

“dirty” form of cell death characterized by swelling and rupture of cell membrane (cell lyse) which causes inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

APOPTOSIS?

A

“clean” form of cell death that does not cause an inflammation
-APOPTOTIC BODIES containing DAMPs are removed by Mf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do DAMPs Activate NF-kB?

A

HMGB1, released by necrotic cells
-activates NF-kB via • via TLR2/TLR3

URIC ACID is another diffusible “danger signal” that:
- Activates NF-kB • via NLRP3

HEAT SHOCK PROTEINS are cytoplasmic proteins serving as DAMPs and

triggering:
- Activates NF-kB via TLR2/TLR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what do all damps stimulate?

A

All DAMPs stimulate production and

release of TNF-a and IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

auto immune diseases and damp?

A

instigate innate immune pathways that promote adaptive autoimmune responses against self-Ags which manifest as severe clinical symptoms
-ex:diabetes 1, lupus, arthiritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

PRINCIPAL SEQUELAE of damps?

A

microbial/sterile stimuli > tissue injury > necrosis and release of DAMPs > DAMPs recognition by PRRs of innate immunity > activation of the innate immune system > infective/sterile inflammatory response > activation of adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is Mannose Receptor? relevance?

A

is a PRR that recognizes glycan with a terminal mannose

-no glycans with terminal mannose in humans, recognize non self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TLR that recognize extracellular pathogens?

A

TLR-1, -2, -4, -5, -6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TLR that recognize intracellular pathogens?

A

TLR-3, -7, -8,-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Endosomal TLRs?

A

respond only to nucleic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how does signalling my TLR work?

A

TLRs activate TRANSCRIPTION FACTORS that stimulate expression of cytokines and other mediators

  • nuclear Factor-κB (NF-kB) which promotes expression of various cytokines and endothelial adhesion molecules
  • Interferon Regulatory Factors (IRFs), which stimulate production of the antiviral cytokines IFN-a/b called type I interferons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

TLR for bacteria?

A

1,2,4,5,9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TLR for viruses?

A

3,7,8,9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

TLR for fungi?

A

2, 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

NLRP3 INFLAMMASOME IN GOUT, why is it relevant?

A

-IL-1β as a key regulatory proinflammatory cytokine in gout,
promoting a neutrophil influx into the synovium and joint fluid
-Anti-IL-1 therapy is used to treat gout patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Signaling Pathways of TLRs?

A

MyD88: adaptor protein

TRIF : makes interferon b

IRF : transcriptional factor

NF-kB***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

TLR DEFICIENCIES? relevance?

A

TLRs are defective, the innate immune cell cannot kill the microbe and patients with these defects present with recurrent infections
-MyD88 deficiency and IRAK-4 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

functional role of TLR?

A

Influence
adaptive response

Direct antimicrobial
response

Tissue injury

influence Macrophage,
dendritic cell
or monocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what do pamps do?

A

TLRs recognize PAMPs and activate Inflammation

pathogen associated molecular patterns” (PAMPs).

PAMPs are effective indicators of the presence of particular pathogens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

PROPERTIES of PAMP?

A

unique to particular classes of pathogens

cannot be altered, suppressed, or hidden from the surface

no structural similarity with self Ags

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

properties of prr?

A

Mannose Receptor is a PRR that
recognizes glycan with a terminal
mannose, no glycans like this in humans

Germ-line encoded

all cells have receptors with
identical specificities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are TLR?

A

recognize microbes by forming pairs with each other. After
recognizing PAMPs on the microbe, the TLRs begin a series of
chemical reactions that allow signals to enter the innate
immune cell and allow it to function in the killing of the
microbe.

37
Q

TLR1/2

TLR2/6

A

bacteria such as

those that cause tuberculosis

38
Q

TLR7, 8 and 9

A

viruses such as hiv and flu

39
Q

NOD-Like Receptors (NLRs) ?

A

PAMPs activate cytoplasmic complexes called INFLAMMASOMES containing these

NLRs act as SCAFFOLDING PROTEINS that assemble signaling platforms
triggering activation of NF-kB and mitogen-activated protein kinase
(MAPK) signaling pathways.

activate caspase 1

40
Q

what is caspase 1?

A

make IL-1β and IL-18

drive inflammation

41
Q

PRR-Triggered Responses in
Phagocytes

say the relevance

A

fMet is in prokaryotes but not eukaryotes

Typical pamp

Macrophages use fMet to distinguish self from nonself

fMet receptor is a PRR belong to the class of G proteincoupled receptors involved in
chemotaxis

PHAGOCYTIC CELLS can bind bacterial proteins starting with fMet, and use them to initiate phagocytosis

42
Q

In innate immunity, macrophages? state any relevant cytokines

A

1.RESPOND TO DANGER SIGNALS
activation of of monocytes/macrophages:
IFNy, TNFa, IL1, IL6

2.REGULATE EXTRAVASATION
chemotaxis:
TNFa, IL1, IL8

  1. Degradation of foreign material, bacteria, and cell debris by PHAGOCYTOSIS and TISSUE REPAIR by secreting various enzymes
  2. INFLAMMATORY MEDIATORS:
  3. ANTIGEN PRESENTATION to effector T cells

6.IMMUNOMODULATION
Il10, il12

43
Q

how do macrophages lead to t cell activation?

A

present Ags to helper T lymphocytes at the sites of infection that leads to T cell activation and production of cytokines that further activate the Mf

44
Q

Mast cells do what in innate immunity?

A

express receptors for many PAMPs and DAMPs

can amplify or suppress innate or acquired immune responses.

common at sites in the body that are exposed to the external environment, such as the skin

regulate vascular permeability and recruitment of blood cells

45
Q

Mast cells, initial and secondary response?

A

begin to produce lipid-derived eicosanoid mediators in the initial minutes of activation, as transcription is not required for these mediators to be converted to an active form.

In a second wave of the response, mast cells begin to release de novo synthesized mediators, including a large number of cytokines such as TNF and IL-4.

46
Q

activators of mast cells?

A

IgE + Ag PAMPs Cytokines Chemokines C3a & C5a complement

47
Q

effectors of mast cells?

A

:Histamine Proteases Serotonin Heparin Cytokines IL-4 & TNF

48
Q

CLASSICALLY ACTIVATED M1?

A

Mf are induced by microbial products binding to TLRs and cytokines, particularly IFN-γ, and are MICROBICIDAL and PROINFLAMMATORY

49
Q

ALTERNATIVELY ACTIVATED M2 Mf?

A

induced by IL-4 and IL-13 and are important in TISSUE REPAIR and FIBROSIS

50
Q

Cytokines , what are they?

A

produced by immune cells mediate inflammation, immunity, and hematopoiesis

51
Q

INNATE IMMUNITY are sub-divided into what two classes

A

– Pro-inflammatory cytokines (stimulate inflammation)

– Anti-inflammatory cytokines (inhibit inflammation)

52
Q

what are chemokines?

A

small protein chemoattractants important for trafficking of immune cells

53
Q

what are Il10, Il18?

A

secreted by macrophages, inhibit inflammation

54
Q

IFNy:?

A

activates macrophages

55
Q

IL12

A

activate NK cells, CD4 becomes Th cells

56
Q

IL8

A

attracts neutrophils, basophils, t cells to infection site

57
Q

Il6

A

activate lymphocytes, cause acute phase proteins, cause fever

58
Q

TNFa

A

increases vascular permeability, increased entry of IgG, complement, fever, shock

59
Q

IL1:

A

synthesis of acute-phase proteins in liver, activate production of Il6 and fever

60
Q

SICKNESS BEHAVIOR SYNDROME what is it?

A

includes lethargy, depression, anorexia, fever

Systemic release of TNF-a, IL-1, and IL-6

61
Q

steps in complement activation?

A

Step 1: C3 convertase made

Step 2:Formation of C5 convertase

Step 3: Formation of membrane attack complex

62
Q

how is step 1 of complement, C3 convertase made?

A
  1. C1 binds to IGM or 2IGG, activated
  2. Activated C1 cleaves both C2 and C4
  3. C4b binds to microbial surfaces
  4. C2a binds to the surface-attached C4b and the C4bC2a C3 convertase is formed
  5. C3 convertase cleaves off the C3a fragment of C3 and generates C3b
63
Q

C3a role?

A

Inflammation & chemotaxis

64
Q

C3b role?

A

Phagocytosis & formation of C5 convertase

65
Q

Step 2 of complement?

A

Formation of C5 convertase

C3b fragment can be deposited on to the surface of bacteria, serves as opsonin to increase phagocytosis

C3 convertase becomes C5 convertase after incorporating the second molecule of C3b

66
Q

Step 3 of complement?

A

Formation of membrane attack complex

  1. The C5 convertase cleaves C5 into the active C5a and C5b fragments.
  2. The C5b fragment is responsible for initiating the self-assembly of the MAC (lytic pathway).
  3. The C5a anaphylatoxin is a potent mediator of inflammatory responses.
  4. The MAC is a supramolecular organization of molecules that contains C5b, C6, C7, C8, together with numerous molecules of C9.
  5. The MAC is responsible for creating the transmembrane channels that lead to cell lysis.
67
Q

what cytokines induce of the acute phase response?

A

IL-6, IL-1, and TNF-a

they act on hepatocytes in the liver, inducing them to secrete APR proteins at higher levels

68
Q

what allows more accurate detection of inflammation?

A

High blood concentrations of CRP and SAA

69
Q

Neutrophils and monocytes can go to site of infection how?

A

without being recruited

70
Q

what is the significance of shear in capillaries?

A

Shear in capillary high, prevent adhesion, low charge in venule

71
Q

steps of neutrophil movement into tissue?

A

Step I: Tethering “rolling”
Step II: Tight binding “Adhesion”
Step III: Diapedesis
Step IV: Chemotaxis – IL-8 controls migration of neutrophils

72
Q

what is the process that allows neutrophil to migrate?

A
  • proinflammatory cytokines TNF-a and IL-1 produced by activated mast cells and tissue resident Mf induce activation of endothelial cells
  • ECs increase surface expression of P selectin (PS) and E-selectin (ES) adhesion molecules.
  • PS and ES bind to their ligands (co-receptors) (PSGL-1) and (ESL-1), respectively, which are constitutively expressed on neutrophils.
73
Q

how does neutrophil binding occur?

A

LFA1 and VLA4 attach to receptors on neutrophils

Bind to ICAM-1 VCAM-1 on activated endothelial cells

Crawling neutrophils follow the chemokine gradient along endothelium, which guides them to the preferential sites of transmigration

74
Q

what is the significance of MCP-1?

A

is the most important chemokine that regulates migration and infiltration of monocytes into the tissues.

75
Q

what is maturation of monocyte controlled by?

A

CYTOKINE MICROENVIRONMENT

76
Q

Eselectin?

A

capture leukocytes

77
Q

Adhesion, crawling and transmigration depend on what?

A

integrins

78
Q

what causes conformotional changes on integrins?

A

iL8 binding with iL8 receptor

79
Q

how does phagocytosis of microbes work?

A
  • microbe binds to phagocyte receptors,ingested in phagosome

- microbes killed in phagolysosome

80
Q

what Oxygen-dependent intracellular killing , how is it relevant to phagocytosis?

A

byproduct of the respiratory burst that accompanies phagocytosis

  1. Oxygen consumption is increased.
  2. Superoxide anion is produced
  3. Hydrogen peroxide (H202 ) production is increased, broken down by catalase
  4. Singlet oxygen
  5. Hydroxyl radicals are produced, react with most organic molecules
  6. Myeloperoxidase, toxic peroxidation
  7. Hypochlorite, the product of the myeloperoxidase enzyme, is more antimicrobial
81
Q

what do type 1 interferons do to stop viruses?

A
  1. TYPE I INTERFERONS (a/b IFNs) block viral replication within host cells.
    induce expression of proteins that interfere with virus replication

a. Protein kinase RNA-activated (PKR) prevents the recycling of guanidine diphosphate which in turns blocks viral RNA translation
b. Type I IFNs activate nuclease Ribonuclease L: rna degradation
c. Type I IFNs directly activate NK cells to enhance their cytotoxicity

82
Q

what do NK cells do to kill virus-infected cells

?

A
  • RECOGNIZE LIGANDS on infected cells or cells undergoing other types of stress, eliminates them
  • The ability of NK cells to kill infected cells is inversely related to expression of MHC class I on the target cells.
  • NK Cells Produce IFN-g That Stimulates Phagocytosis by Mf
  • NK cell ACTIVATING RECEPTORS are called killer cell immunoglobulin (Ig)-like receptors (KIRs) that recognize stress-associated molecules (e.g., MICA and MICB in humans)
  • INHIBITORY RECEPTORS recognize class I MHC and activate protein tyrosine phosphatases (PTP) inhibit an activation signal
  • KIR-MHC I binding occurs, the NK cell will proceed to kill the target host cell.
83
Q

How does NK cell kill infected cells?

A
  1. perforins
  2. granzyme
  3. apoptosis
  4. macrophages
84
Q

microbial resistance to phagocytosis?

A

Capsular polysaccharide

85
Q

microbial resistance to ROS?

A

Production of catalase

86
Q

microbial resistance to complement?

A

Sialic acid to inhibit c3 and c5 convertase

M protein to block c3 binding

87
Q

microbial resistance to antibiotics?

A

Modified LPS that blocks antibiotics

88
Q

two signals that innate immune system uses to start adaptive?

A
  1. Recognition of ANTIGEN by T lymphocytes
  2. Regulatory molecules expressed on Ag-presenting cells (i.e., dendritic cells and Mf) are called COSTIMULATORY MOLECULES

“Signal 3” provided by cytokines

89
Q

how does innate immunity indirectly control Ab mediated responses of adaptive immunity?

A

bridge between innate and adaptive immunity

PRRs cause activation and maturation of antigenpresenting cell (APC).

APC processed antigen is presented to naïve T cells
Secreted CYTOKINES assist the development and maturation of T-cell

MCM Quiz2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions