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IHL Exam 1 > Innate immunity (Bowden) > Flashcards

Innate immunity (Bowden) Flashcards

1
Q

Which type of immunity will recognize molecular patterns and which recognize microbial molecules such as antigens

A

innate- molecular patterns.

Adaptive- specific antigens on microbes

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2
Q

Describe the difference of where the R originate from in innate vs adaptive immunity

A

innate- germline- limited diversity

encoded by genes produced by somatic recombination of gene segments- greater diversity

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3
Q

Describe the distribution of R in innate and adaptive immunity

A

innate- nonclonal, identical R on all cells of same lineage

adaptive- clonal, clones of lymphocytes with distinct specificities and R

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4
Q

Which type of immunity can discriminate between self and non self

A

both

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5
Q

What does IL-3 convert a pluripotent stem cell into

A

myeloid and lymphoid progenitors

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6
Q

What is IL-7 role in hematopoiesis

A

commitment to lymphoid lineages (B and T cells), made by BM stromal cells,

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7
Q

What converts a myeloid progenitor cell NOT into a RBC

A

IL3, GM-CSF, IL1 and IL6

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8
Q

What commits myeloid to megakaryocyte

A

thrombopoietin and IL-11

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9
Q

what commits myeloid to eosinophil

A

IL-5

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10
Q

What commits granulocyte-monocyte CFU to neutrophil?

A

IL-3 GM-CSF and G-CSF

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11
Q

What commits granulocyte-monocyte CFU into monocyte?

A

IL-3, GM-CSF, M-CSF

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12
Q

What are PMNs

A

neutrophils, polymorphonucleated because the nucleus has 2-5 lobes

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13
Q

What are the R for neutrophils

A

IFNgamma, chemokines, TLRs, Complement, Mannose, scavenger, FcR IgG

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14
Q

What leukocyte is first at site of infection and what takes days

A

neutrophils- hours

macrophages-days

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15
Q

2 types of Macrophages

A

Inflammatory and Resident

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16
Q

What shape nucleus is in a macrophage

A

u shaped

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17
Q

R for macrophages

A

TLRs, Scavengers, N-formyl Met-Leu-Phe, Fc, Complement, Mannose, Integrins, IFNgamma and chemokines

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18
Q

What activates macrophages

A

phagocytosis, opsonization, ROS, iNOS, Cytokines, GF

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19
Q

What is the role of the N-formylmethionyl R on macrophages

A

Migration into tissues

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20
Q

What is the role of the mannose R onmacrophages

A

phagocytosis

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21
Q

What are the rolls of TLRs and Cytokine Rs on macrophages

A

ROS,iNOS,cytokines TNF and IL-12, Fibroblas growth factors, angiogenic factors, metalloproteinases

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22
Q

How do NK cells work on macrophages?

A

secrete IFN gamma which activates macrophages

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23
Q

How do macrophages work on NK cells?

A

secrete IL-12 to activate NK

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24
Q

What principal mediator of ADCC do NK activate

A

IgG Fc

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25
Q

inhibitory R of NK cells

A

class I MHC

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26
Q

How do NK cells get into cell to cause apoptosis

A

granzymes then perforins

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27
Q

What receptors are constitutively active on NK surface

A

activating and inhibitory

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28
Q

Two types of Mast cells

A

tissue and mucosal

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29
Q

What stimulates mast cells

A

direct injury, chemical alcohols, and certain antibiotics, cross linking of IgE R or by activated complement proteins

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30
Q

What is in the immediate release of mast cell granules

A

histamine, protesases, heparin, TNF

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31
Q

What is made in membrane derived lipid mediators over minutes in mast cells

A

PGs, leukotrienes,platelet activation factor(PAF)

32
Q

what cytokines are produced in mast cells

A

IL- 1 IL3 IL4 IL5 IL6 IL8 and TNF

33
Q

What causes the differentiation of eosinophils

A

IL5

34
Q

What was the original purpose of eosinophils

A

multicellular parasites, now do everythign

35
Q

Dendritic cells (APC)

A

pick up antigen for processing, long dendritic processes. bridge between innate and adaptive

36
Q

2 types of APCs

A

conventional and plasmacytoid

37
Q

Fucntions of epithelia

A

physical and chemical barrier, normal flora, specialized lymphocytes

38
Q

functions of mucosal surfaces

A

removal of particles, rapid pH buffer, mucus/secretions, cilia, normal flora

39
Q

Defensins characteristics

A

tiny aa sequences. + charged. widely distributed. B sheets and 6 di-S bonds

40
Q

Defensins antimicrobial activities

A

Gram - and + bacteria, fungi(yeasts), parasites, viruses

41
Q

What are defensins produced by?

A

neutrophils, lymphocytes, paneth cells, epithelial cells and keratinocytes

42
Q

PAMPs

A

Pathogen-associated Molecular Patterns

recognition of microbes

43
Q

Where PAMPs found

A

on molecules and structures on a variety of microbes but not self molecules. MAIs and Danger Signal

44
Q

structures microbes need to survive and infect

A

LPS(OPS), mannose residues, dsRNA

45
Q

What are DAMPs

A

Damage associated Molecular Patterns.

recognize necrosis

46
Q

What is an example of a DAMP

A

Alamins

47
Q

What do DAMPs cause

A

TLR signaling through NF-kB activation

48
Q

Increased levels of DAMPs have been assoc with what type of disease?

A

inflammatory diseases like sepsis, arthritis, atherosclerosis, lupus, crohn’s, cancer

49
Q

How do we recognize PAMPs and DAMPs? Where are these R encoded?

A

Pattern Recognition Receptors- germline encoded

50
Q

What are the signaling pathways of TLRs

A

NFkB, AP1 IRF3 IRF5

51
Q

What genes do TLRs upregulate

A

TNF, IL1b IL6 IL8 and IL12 and e selectin

52
Q

What is the net result of activated TLR

A

increase in microbial activity and apoptosis, production of defensins, expression of co-stimulatory molecules

53
Q

What are NOD Receptors and what do they bind to

A

Intracellular TLRs, recognize PAMPs no viruses and some bacteria

54
Q

What is the general cascade of tLR

A

recruitment of adaptor proteins->recruitment and activation of protein kinases-> activation of transcription factors-> gene transcription and then expression of inflammatory cytokines, chemokines, e selectin etc

55
Q

What cytokines are major pyrogens

A

TNF and IL1

56
Q

primary role of chemokines

A

increase integrin affinity and chemotaxis

57
Q

Where is IL12 produced and what does it cause

A

produced in dendritic cells and macrophages to act on NK and T cells to increase IFNgamma production.
cause T cells to differentiate into T helper cells

58
Q

Type I IFNs where are they found. and what do they do

A 
alpha:dendritic and macrophages. beta:fibroblasts
Causes all cells to increase class I MHC expression and activates NK
59
Q

Where is IL10 made what what are its affects

A 
macrophages, dendritic cells, T cells
inhibits IL12 production and reduces expression of class II MHC molecules
60
Q

What does IL6 do and where is it produced

A

causes liver to produce acute phase proteins.
causes B cells to create many ab
made in macrophages endothelial cells and T cells

61
Q

What does IL 15 do and where is it produced

A

causes proliferation of NK and T cells, produced by macrophages

62
Q

Where is IL18 produced and what effect does it have

A

macrophages

targets: NK cells and T cells and IFNgamma production

63
Q

What are the mechanisms of immune evasion

A

resistance to phagocytosis, resitance to ROS in phagocytes, resistance to complement activation, resistance to antimicrobial peptide antibiotics

64
Q

3 key parts to acute inflammatory response

A

vasodilation, increased vascular permeability, emigration of leukocytes from bottom into the damaged area

65
Q

what signaling molecules increase permeability

A

Histamine, bradykinin, C5a, leukotriene-B4, f-met-leu-phe, platelet-activating factor

66
Q

What proteins are involved in inflammatory exudate (edema)

A

clotting proteins, fibrinolytic protein, complement system, kinin cascade

67
Q

what is the kinin cascade in Edema

A

vasodilation, increase permeability of blood vessels and stimulates pain receptors

68
Q

What molecules increase expression of P and E selectins

A

IL1 and TNF

69
Q

how to P and E selectine recruit leukocytes

A

leukocytes bind, dettach and roll until they are slowed down and can react to chemokines. Reaction involves flattening and entering endothelium.

70
Q

What receptor stops neutrophils from rolling away

A

ICAM1

71
Q

What receptor stops macrophages from rolling away

A

VCAM1

72
Q

3 possible outcomes of capillary damage

A

Chronic inflammation, fibrosis or resolution

73
Q

Leukocyte Adhesion Deficiency LAD

A

Leukocytes cannot leave the vasculature to migrate to tissues during inflammation/infection

74
Q

b2 chains of integrins or CD18 deficiency

A

LAD1 because little to no surface membrane expression of LFA1, Mac1 or gp150/95

75
Q

what is the inheritance mode of LAD 1

A

autosomal recessive

76
Q

Clinical presentation of LAD 1

A

delayed separation of the umbilical cord and omphalitis
recurrent bacterial infections of skin and mucosa
leukocytosis
periodontitis
impaired wound healing
absent pus formation

IHL Exam 1 (11 decks)

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