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Immunology > 52-Granulocytes and Protein Components > Flashcards

52-Granulocytes and Protein Components Flashcards

1
Q

Overactive granulocyte activation

A

Allergic symptoms

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2
Q

Overactive pathogen sensing receptors

A

Autoimmune disorders

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3
Q

Defects in protein components

A

Increased risk of infection

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4
Q

granulocytes

A

eosinophils, basophils, mast cells

Contains large granules that are released non specifically upon activation

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5
Q

What do granulocytes protect

A

Epithelial and mucosal surfaces from multicellular parasites and mucosal pathogens

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6
Q

Role of mast cells

A

Sentinels

Recruit eosinophils and basophils

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7
Q

Activation of mast cells

A

Production of IgE antibodies from antibody producing B cells after encountering pathogen
IgE antibodies bind Fc epsilon receptor to release histamine

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8
Q

Activation of eosinophiles

A

Priming with cytokines, soluble Its, or pattern recognition receptor ligans
Activation with immobilized Its, microbial produces, interim engagement, cytokine mediators

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9
Q

Function of inflammatory mediators

A

Create hostile environment for pathogens that are too big to eat
Directly kill pathogen
Further activate immune response

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10
Q

Function of histamine

A

Alter smooth muscle contraction, vascular permeability, and neuron function

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11
Q

Inflammatory mediators

A 
Histamine
Protease and antimicrobial peptides-kill pathogens
Lipid mediators
Cytokines-alter function of immune cells
chemokines-recruit other cells
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12
Q

Inappropriate granulocyte function

A

Linked to human disease

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13
Q

What causes allergies and asthma

A

eosinophils and mast cells

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14
Q

Drugs that inhibit granulocyte function

A

Antihistamines
anticytokine drugs
NSAIDS
croticosteroids

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15
Q

Type 1 interferon release

A

Antiviral response
Detected by toll like and RIG-I receptors
Induction of genes encoding type 1 IFNs
Release of IFN into environment and binding to receptor

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16
Q

What happens after IFN bind receptor

A

Activation of downstream signaling pathways JAK/STAT

Induction of IFN stimulated genes (ISGs)

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17
Q

What drives the transcription of type 1 INF

A

IRF3, IRF7, NF-kB, and MAP kinase pathways

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18
Q

Function of IFN

A

Upregulated ISG
Stimulate antigen presenting cells
Enhance functions of NK, T, and B cells

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19
Q

What does up regulation of ISG do

A

Suppress viral function by blocking replication cycle

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20
Q

What does stimulation of antigen presenting cells do

A

produce inflammatory cytokines and enhance presenting function

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21
Q

What do NK, T and B cells do

A

NK and T-target and kill

B-produce antibodies

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22
Q

defensins

A

Small antimicrobial agents
Positively charged
Bind to negative pathogen membrane
Form pore to destroy pathogen

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23
Q

cathelicidins

A

Small antimicrobial agents
Positively charged
Bind to negative pathogen membrane
Form pore to destroy pathogen

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24
Q

Where are defensins and cathelicidins found

A

Neutrophils, macrophages, mast cells
paneth cells
keratinocytes

25
Q

Defensins and cathelicidin in neut, mac, and mast

A

In primary and secondary granules

26
Q

Defensins and cathelicidins in paneth cells

A

In crypts of small intestine
Large quantities of defensisns
Suppress growth of commensals and pathogenic in mucosal tissue

27
Q

defensisns and cathelicidns in keratinocytes

A

Decrease the growth of pathogens on the surface of the skin

28
Q

Collectins

A

antimicrobial
form trimer with ficolin and then higher order complex
increase phagocytosis or complement binding

29
Q

ficolins

A

antimicrobial
form trimer with collectins and then higher order complex
increase phagocytosis or complement binding

30
Q

antimicrobial proteins

A

ficolins
Surfactants
Mannose binding lectins
collectins

31
Q

function of collectins and ficolins

A

form trimers and higher order complex to increase phagocytosis and complement binding

32
Q

avidity effect

A

increase affinity of entire complex by forming higher order structures

33
Q

what do ficolins bind to

A

N acetyl glucosamine

34
Q

what do mannose bind to

A

mannose derivatives

35
Q

what do surfactants A and D bind to

A

mannose and glucose derivatives

36
Q

what do human glycoproteins contain

A

galatose, fructose, and sialic acid

37
Q

how do collectins and ficolins find pathogens

A

different sugars on surface than humans
n acetyl glucosamine, mannose, glucose
vs.
galatose, fructose, sialic acid

38
Q

complement system

A

30 proteins produced by liver
protein pathway in the innate response
kill pathogens and enhance immune function

39
Q

what increases expression of complement protiens

A

infection and inflammation

40
Q

3 methods of complement activation

A

lectin, classical, alternative

41
Q

4 outcomes of complement activation

A

inflammation and chemoattraction
phagocytosis
membrane attack complex
antibody production

42
Q

common complement cascade starting at C3

A

C3 cleavage into C3a and C3b
C3b stays on pathogen and coats it to enhance phagocytosis (opsinization)
C3b recruits C5 and cleaves into C5a and C5b
C5b recruits C6, 7, 8, 9
C9 forms a pore
C3a and C5a function as inflammatory mediators and chmoattractans

43
Q

membrane attack complex

A

formed from polymerization of C9, bursting pathogen cells
effective against gram negative and enveloped virus
gram positive is immune

44
Q

activators of classical pathway

A

antibodies IgM, IgG1, IgG3, or pentraxin

IgA and IgE do not activate

45
Q

steps in classical pathway

A

binding of antibody/pentraxin recruit C1 complex (C1q, C1s, C1r)
recruitment of C1 complex cleaves C4 into a and b
C4b binds and cleaves C2
C4b/C2b complex serves as C3 convertase complex

46
Q

pentraxins

A

proteins found in blood that resemble antibodies

C reactive protein

47
Q

C1q

A

classical pathway

binds antibodies or pentraxin

48
Q

steps in lectin pathway

A

activated by collectins or ficolins which are bound to MASP 2 and 3 which cleave C4
C4b stays and binds C2 which gets cleaved
C4b/C2b form C3 convertase complex

49
Q

activators of lectin pathway

A

collectins or ficolins to sugar residues

50
Q

steps in spontaneous activation pathway

A

C3 spontaneously cleaved by water, C3b binds to nearest surface
C3b binds complement factor B which cleaves into Bb and Ba
C3b/Bb form C3 convertase complex

51
Q

goals of spontaneous activation pathway

A

amplify classical and lectin pathways

antibody independent pathway

52
Q

regulators of classical and lectin complement pathway

A

C1 INH, C4bp inhibit C1 complex and C4b

53
Q

regulators of spontaneous complement pathway

A

Cr1, DAF, MCP on surface of cells and factor H and I in blood

54
Q

lack of complement proteins

A

increased bacterial infections

55
Q

deficiencies of proteins in classical pathwya

A

autoimmune disorders

56
Q

polymorphisms in suppressive factors

A

age related macular degeneration

atypical hemolytic uremic syndrom

57
Q

deficiency in what factors cause increased susceptibility to infections

A

B, D, 3, 5, 6, 7, 8, 9

especially Neisseria

58
Q

deficiency in what factors cause disease that resembles lupus

A

1, 2, 4

Immunology (19 decks)

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