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Immunology & Serology > IMMUNOSERO // STEVENS CHAP 3: INNATE IMMUNITY > Flashcards

IMMUNOSERO // STEVENS CHAP 3: INNATE IMMUNITY Flashcards

1
Q

Consists of the defenses against infection that are ready for immediate action when a host is attacked

A

Innate immunity

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2
Q

10% to 15% of total cell pop. in tissues; most important cells in pathogen recog.

A

Macrophages & Dendritic

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3
Q

are able to distinguish pathogens from normally present molecules in the body

A

Macrophages & Dendritic

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4
Q

discovery of the first receptor in humans, the Toll-like receptor (TLR); major impact on the understanding of innate immunity.

A

Charles Janeway

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5
Q

Protein originally discovered in fruit fly Drosophila;plays important role in antifungal immunity in adult fly.

A

Toll

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6
Q

Highest conc. of these TLRs: on

A

monocytes, macrophages, & neutrophils

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7
Q

Membrane-spanning glycoproteins; share a common structural element called

A

leucine-rich repeats (LRRs)

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8
Q

Once TLRs bind to their particular substances, host immune responses are rapidly activated by production of

A

Cytokines and chemokines

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9
Q

Plasma membrane receptors found on mono, macrophages, dendritic cells, neuts, B cells & T-cell subsets.

A

C-type lectin receptor (CLR)

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10
Q

C-type lectin receptor (CLR) bind to_______ found in fungal cell walls.

A

mannan and β-glucans

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11
Q

Recognizes RNA from RNA virus in the cytoplasm of infected cells

A

Retinoic acid-inducible gene-I-like receptors (RLRs)

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12
Q

Induces inflammatory cytokine and type I interferons.

A

Retinoic acid-inducible gene-I-like receptors (RLRs)

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13
Q

inhibit viral replication and induce apoptosis (cell death) in infected cells.

A

Type I interferons

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14
Q

Bind peptidoglycans found in bacterial cell walls; also protect against intracellular protozoan parasites

A

Nucleotide-binding oligomerization domain receptors (NOD)

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15
Q

Mutations in NOD receptors; a painful inflammatory disease of the bowel.

A

Crohn’s disease

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16
Q

Normal serum constituents that increase rapidly because of infection, injury, or trauma to the tissues.

A

ACUTE-PHASE REACTANTS

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17
Q

Many act by: binding to microorganisms and promoting adherence, the first step in phagocytosis.

A

ACUTE-PHASE REACTANTS

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18
Q

help to limit destruction caused by the release of proteolytic enzymes from WBCs as the process of phagocytosis takes place.

A

ACUTE-PHASE REACTANTS

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19
Q

particular cytokines involved
All of which are produced by monocytes and macrophages at the sites of inflammation.

A

Interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)

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20
Q

A trace constituent of serum originally thought to be an antibody to the C-polysaccharide of pneumococci.

A

C-REACTIVE PROTEIN (CRP)

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21
Q

C-REACTIVE PROTEIN (CRP) was discovered by

A

Tillet and Francis in 1930

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22
Q

acts somewhat like an antibody because it is capable of opsonization (the coating of foreign particles), agglutination, precipitation, and activation of complement by the classical pathway.

A

C-REACTIVE PROTEIN (CRP)

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23
Q

Promotes phagocytosis by binding to specific receptors found on monocytes, macrophages, and neutrophils.

A

C-REACTIVE PROTEIN (CRP)

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24
Q

can be thought of as a primitive, nonspecific form of an antibody molecule that is able to act as a defense against microorganisms or foreign cells until specific antibodies can be produced

A

C-REACTIVE PROTEIN (CRP)

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25
Q

the most widely used indicator of acute inflammation.

A

C-REACTIVE PROTEIN (CRP)

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26
Q

CRP concentration of Normal levels in adults

A

0.47 to 1.34 mg/L

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27
Q

It is an apolipoprotein that is synthesized in the liver and has a molecular weight of 11,685 daltons.

A

SERUM AMYLOID A (SAA)

28
Q

Normal circulating levels of SAA

A

5 to 8 ug/mL

29
Q

Act as a chemical messenger, similar to a cytokine

A

SERUM AMYLOID A (SAA)

30
Q

Activates monocytes and macrophages to then produce products that increase inflammation

A

SERUM AMYLOID A (SAA)

31
Q

Refers to a series of serum proteins that are normally present

A

Complement

32
Q

Overall function: mediation of inflammation

A

COMPLEMENT

33
Q

Major functions of complement:

A

(1) Opsonization,
(2) Chemotaxis/Inflammation and
(3) Lysis of cells.

34
Q

A 52-kD protein that is primarily synthesized in the liver.

A

ALPHA1-ANTITRYPSIN (AAT)

35
Q

The major component of the alpha band when serum is electrophoresed.

A

ALPHA1-ANTITRYPSIN (AAT)

36
Q

it’s a general plasma inhibitor of proteases released from WBCs

A

ALPHA1-ANTITRYPSIN (AAT)

37
Q

Enzyme secreted by neutrophils during inflammation that can degrade elastin & collagen

A

Elastase

38
Q

Acts to “mop up” or counteract the effects of neutrophil counteract the effects of neutrophil

A

AAT

39
Q

It also regulates expression of proinflammatory cytokines limiting harmful side effects of inflammation

A

AAT

40
Q

can also react with any serine protease

A

AAT

41
Q

Generated by the triggering of the complement cascade or fibrinolysis

A

Serine proteases

42
Q

An alpha2-globulin with a molecular weight of 100,000 daltons.

A

HAPTOGLOBIN

43
Q

It binds irreversibly to free hemoglobin released by intravascular hemolysis.

A

HAPTOGLOBIN

44
Q

Acts as an antioxidant to provide protection against oxidative damage mediated by free hemoglobin.

A

HAPTOGLOBIN

45
Q

Normal plasma concentrations range of haptoglobin

A

40 to 290 mg/dL.

46
Q

An acute-phase protein involved in the coagulation pathway

A

FIBRINOGEN

47
Q

A small portion is cleaved by thrombin to form fibrils that make up a fibrin clot.

A

FIBRINOGEN

48
Q

makes blood more viscous and serves to promote aggregation of RBCs and platelets.

A

Fibrinogen

49
Q

It is the principal copper-transporting protein in human plasma, binding more than 70% of the copper found in plasma by attaching 6 cupric ions per molecule.

A

CERULOPLASMIN

50
Q

Also acts as an enzyme, converting the toxic ferrous ion (Fe2+) to the non-toxic ferric form (Fe3+)

A

Ceruloplasmin

51
Q

A depletion of ceruloplasmin

A

Wilson’s disease

52
Q

Autosomal recessive genetic disorder characterized by a massive increase of copper in the tissues.

A

Wilson’s disease

53
Q

Serum proteins that attach to a foreign cell or pathogen and help prepare it for phagocytosis.

A

Opsonins

54
Q

May act by neutralizing surface charge on foreign particle, making it easier for cells to approach one another

A

Opsonins

55
Q

a powerful oxidizing agent and is highly toxic for microorganisms. It is the main component of household bleach used to disinfect surfaces

A

Hypochlorite

56
Q

Kill wide spectrum of organisms, including both gram (+) and gram (-) bacteria, many fungi, and some viruses.

A

Defensins

57
Q

When released from lysosomal granules, able to cleave segments of bacterial cell walls w/o benefit of O2

A

Defensins

58
Q

Another example of a protein that is able to damage bacterial cell membranes.

A

Cathepsin G

59
Q

release various colony stimulating factors that act on developing granulocytes and macrophages. Actions of these, therefore, have a major influence on both innate and adaptive immunity.

A

NK cells

60
Q

2 main classes of binding receptors on NK cells:

Which deliver inhibitory signals

A

Inhibitory receptors

61
Q

main classes of binding receptors on NK cells:

Which deliver signals to activate the cytotoxic mechanisms

A

Activating receptors

62
Q

Examples of activating receptors that bind stress proteins are

A

a. CD16
b. NKG2D

63
Q

If an inhibitory signal is not received when binding to activating receptors occurs, then NK cells release substances called

A

perforins and granzymes

64
Q

Proteins that form channels (pores) in the target cell membrane.

A

Perforins

65
Q

Packets of enzymes that may enter through the channels and mediate cell lysis.

A

Granzymes

Immunology & Serology (13 decks)

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