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Week 2 Phys > 23 Innate immunity > Flashcards

23 Innate immunity Flashcards

1
Q

1) Recognize and eliminate damaged and dead host cells
2) Stimulate the adaptive immune responses and influence the nature of the adaptive response
Are the functions of the ___

A

Innate immune system

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2
Q

Enable recognition of foreign microorganisms

A

Receptors

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3
Q

___ are mounted to eliminate the foreign microorganisms

A

Effector components

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4
Q

o Receptors are encoded in the germline
o Limited diversity
o Pattern recognition receptors (PRRs)
 Recognizes structures shared by various microbes

A

Innate immune system receptors

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5
Q

o Epithelial barriers and secreted antimicrobial proteins are always present and do not need to be activated
o All other components of the innate immune system must be

A

Effector functionsd of the innate immune system

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6
Q

o Activated by sequential proteolysis (activation)
o Activation is inhibited by regulatory proteins that are present on normal host cells and absent from microbes (minimize damage to host cells)

A

Complement system

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7
Q

Cleaves complement component 3 (C3), which releases C3b and C3a as products.

A

C3 convertase

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8
Q

Stimulates mast cell degranulation, thus triggering an immune response. Attracts phagocytic cells to the site of inflammation

A

C3a

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9
Q

• The larger of the two elements formed by the cleavage of complement component 3. ___ covalently bonds to microbial cell surfaces within an organism’s body. Binds with the C3 convertase, forming the C5 convertase

A

C3b

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10
Q

Cleaves complement component 5 (C5), releasing C5a and C5b as products

A

C5 convertase

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11
Q

Diffuses away from the C5 convertase reaction and attracts phagocytic cells to the site of inflammation

A

C5a

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12
Q

Stays bound to the surface of the microorganism and continues the complement cascade (ends with the creation of a pore in the surface of the microorganism –the membrane attack complex)

A

C5b

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13
Q

Allows liquids, electrolytes, and other cellular components to exit/enter the microorganism, causing cell lysis

A

Membrane attack complex (MAC). Note: formation of the MAC is not effective against microorganisms that have a protective layer of carbohydrates, or an extra-thick membrane

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14
Q

Loss of liver function (e.g. alcoholic cirrhosis or chronic hepatitis B) leads to decreased complement protein synthesis and reduced complement function  patients are predisposed to infections caused by ___ bacteria

A

Pyogenic bacteria

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15
Q

Part of the adaptive immune response (b/c antibodies are necessary to detect antigen on the pathogen surface and eventually form C3 convertase

A

Classical pathway

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16
Q

C3 is normally around (normally hydrolyzed). However, C3 may become attached to the surface of microorganisms, attracting factor B (which gets cleaved and attracts factor D which also gets cleaved). The end cleavage product is the C3 convertase

A

Alternative pathway

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17
Q

The mannose-binding lectin (MBL) is made by the liver. It is able to bind lectin (which is bound to carbohydrates of the microorganism membrane). It attracts C2, and C4, and the end cleavage product is C3 convertase.

A

MB-lectin pathway

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18
Q

Attaches to the surface of the microorganism, attracting C5b, C6, C7, C8, and C9 (forms the membrane attack complex, which lyses the pathogen)

A

C3b

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19
Q

May also be recognized by the C3b receptors of phagocytic cells, causing opsonization and phagocytosis

A

C3b

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20
Q

Allows for removal of antigen-antibody complexes and aids the B cells to identify pathogens

A

Cooperation w/ adaptive immune system

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21
Q

Inactivates protease activity of C1. This inhibits the classical pathway. A deficiency in C1 inhibitors leads to upregulation of the classical pathway (hereditary angioedema). In this disease, there are increased C3a, C4a, and C5a concentrations, leading to excessive inflammation, vasodilation, and vascular permeability, leading to edema

A

C1 inhibitor

22
Q

Disease resulting from upregulation of the classical pathway. There are increased C3a, C3a, and C5a concentrations, leading to excessive inflammation, vasodilation, and vascular permeability, leading to edema

A

Hereditary angioedema

23
Q

Binds to C4b and C4b, limiting the formation of C3 and C5 convertases. A deficiency leads to increase C3 and C5 convertase formation. This leads to complement-mediated hemolysis (paroxysmal nocturnal hemoglobinura is the resulting disease and is due to increased RBC lysis)

A

Decay accelerating factors

24
Q

Disease caused by deficient decay accelerating factor levels, and the resulting increase in C3 and C5 convertase formation

A

Paroxysmal nocturnal hemoglobinura

25
Q

Patients w/ C5-C9 complement deficiencies have increased susceptibility to only certain types of infections ( ___ and ___ infections)

A

Meningococcal & Neisseria-gonorrhea

26
Q

A phagocytic cell w/ a C3b receptor will increase its recognition of the pathogen to which the C3b protein is bound. Note: iC3b or Ab individually will enhance phagocytosis of the pathogen. However, both iC3b and Ab together will enhance phagocytosis of the pathogen even more

A

Opsonization (enhanced phagocytosis)

27
Q

1) Formation of the MAC
2) Opsonization
3) inflammation

A

Functions of the complement system

28
Q

Stimulated by C3a and C5a. All below factors are involved:
 Contraction of smooth muscle
 Increase vascular permeability
 Increase expression of cell-adhesion molecules (CAM) on endothelial cells
 Activate mast cells and basophils to produce inflammatory mediators (i.e. histamine, Tumor necrosis factors (TNFa))
 C5a: acts directly on phagocytic cells to increase adhesion and extravasation

A

Inflammation

29
Q

A variety of ROSs are generated (toxic to microorganisms). Hydrogen peroxide, hydroxyl radicals, activated halides (Cl-, I-, etc), and NO are all used

A

Oxygen dependent killing

30
Q

Lysosomal enzymes and acidic pH destroy the microorganism.

A

Oxygen-independent killing

31
Q

Defect –NADPH oxidase activity (inability to form hydrogen peroxide). Consequence: Lack of oxidative burst and defective bactericidal activity. Leads to buildup of macrophages that are not able to kill microorganisms (granulomas)

A

Chronic granulomatous disease

32
Q

Defect –Myeloperoxidase (lack of hypochlorite production). Consequence: phenotype is mild b/c of the presence of other reactive oxygen species that can handle microorganisms

A

Myeloperoxidase deficiency

33
Q

May be activated by pathogens (lipopolysaccharides and mannose in the microorganism membrane) themselves or by the cells of the immune system.

A

Macrophages

34
Q

A macrophage that has been activated by an antigen will increase in size and in its capacity for phagocytosis. It will also produce and secrete more cytokines that are normally produces by macrohpages

A

Hyperactivated macrophage

35
Q

A macrophage that has been activated by T cells or NK cells (interferin-gamma mediated) will have enhanced expression of antigen presentation (increased expression of MHC2). They will also have increased phagocytic capacity

A

Primed macrophage

36
Q

T/F. Activated macrophages secrete a number of cytokines that promote inflammation (IL-1 and TNF-alpha)

A

True

37
Q

1) Inhibition of fusion w/ the lysosome
2) Prevention of acidification of endosomes
3) Escape the endosome
4) Prevent presentation of antigen
5) Therefore, a bacteria that would’ve normally developed in the extracellular space now develops inside macrophages

A

Mechanisms developed by pathogens to enter and survive inside macrophages

38
Q

o About 70% of cells in the blood (most abundant cells in the blood)
o Shorter half-life compared to macrophages (b/c they are too dangerous to keep around for long)
o Attracted to the site of inflammation by interleukin-1 and TNF-alpha (both are secreted by macrophages), C5a, and by microorganisms (lipopolysaccharides)
o Function: phagocytosis

A

Neutrophils

39
Q

Defect –integrin beta chain/CD18 (type 1) and selectin (type 3). Consequence: poor adhesion of neutrophils to endothelium. Leukocytes also have poor adhesion. Therefore the endothelium is affected (low quality integrin attached) so are several cells involved in the immune response

A

Leukocyte adhesion deficiency

40
Q

The process by which leukocytes and circulating plasma proteins are brought into sites of infection and activated to destroy and eliminate the offending agents

A

Inflammation

41
Q

Function to induce apoptosis in infected host cells (w/ virus, bacteria, or cancerous cells) and damaged cells
o Different than T-CD6 cells in that there is no T-cell receptor (no education)
o Markers: CD16 (Fc-IgG), CD56. Found on the surface of these cells
o Migrate to tissues (roll, stop, enter)
o Recognize target cells by checking the balance b/t kill vs. non kill signals
 Kill signals: e.g. foreign molecules (lipopolysaccharides –LPS)
 Non-kill signals: e.g. MHC1
 Activated by interleukin 2 (IL2 –stimulates proliferation of all T cells), interferon (IFN alpha & IFN beta)
o Cytokine production: e.g. IFN-gamma, for differentiation of Th1 cells (helper T cells)

A

Natural killer cells

42
Q

consists of changes in cells that prevent virus replication and increase susceptibility to killing by lymphocytes, thus eliminating reservoirs of viral infection
o A cell that has been infected by a virus will synthesize interferon which travels to neighboring cells, activating the IFN receptors and thus activating the antiviral response. The below are functions of the antiviral response
 Cells whose IFN receptors have been activated synthesize antiviral proteins that sit in the cytosol. Thus they are “ready for” the invasion of viral proteins and will degrade any viral proteins that end up in their cytosol
o Other functions:
 Increase antigen presentation (increase MHC1 expression)
 Induce chemokine release to recruit lymphocytes
 Activates NKC

A

Antiviral defense

43
Q

The link b/t innate and adaptive immunity
o (NOT macrophages) Take up bacterial antigens in the skin (and tissues) and move to enter a draining lymphatic vessel
o Bearing antigen, these cells enter the draining lymph node where they settle in the T-cell areas

A

Dendritic cells

44
Q

Not formed in host cells b/c of a protective response (specialized molecules) that prevents these holes from forming in the membrane

A

Membrane attack complex

45
Q

As a result of infection, these cells increase in concentration in the blood

A

Neutrophils

46
Q

What is the order in which immune cells are activated during an infection?

A

1) Resident macrophages are activated first
2) Neutrophils are the first cells recruited to the site of infection by macrophage cytokines
3) Monocytes are then recruited so that they can differentiate into more macrophages
4) Lymphocytes are then recruited to deal with the infection

47
Q

___-gamma is involved in the interplay b/t macrophages & NK cells. ___ type-1 (alpha or beta) Is involved in the antiviral response

A

Interferon (IFN)

48
Q
  • Innate immune response: LPSs found on the surface of bacteria can activate the system. Neither antibodies nor T cell receptors are involved
  • Adaptive immune response: The most potent means of activating this sytsem. This occurs when antibodies bind to the antigen at the surface of a cell. This exposes the Fc region of the antibody in a way that allows the first complement protein (C1) to bind
A

Activation of the complement system

49
Q

Complement peptides. Ex: C3a, C4a, and C5a

A

Anaphylatoxin

50
Q

Review the diagrams

A

Do it

Week 2 Phys (17 decks)

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