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Immuno > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

What is the difference between innate and adaptive immunity in terms of time?

A

innate immunity happens immediately, whereas adaptive immunity happens late

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2
Q

Pathogens are usually in 2 compartments. What are they?

A

1) Extracellular-can be taken care of by innate immune system/phagocytes
2) Intracellular-Innate cannot access the pathogens here. Need NK cells and the cytotoxic arm

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3
Q

What are the 2 mechanisms of tissue damage by pathogens?

A

direct and indirect

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4
Q

Viruses _________ the cells that they infect

A

damage

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5
Q

T/F:

Most pathogens can overcome innate immune response and need adaptive response to prevent subsequent infection

A

true

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6
Q

_________ surfaces of the body provide the first barrier against infection.

A

Epithelial

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7
Q

Epithelial surfaces of the body provide the first barrier against infection. What is internal epithelia?

A

mucosal epithelia, secrete mucus made up of glycoprotein mucins * Cystic Fibrosis *

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8
Q

The epidermis of the skin has multiple layers of ________________ in different layers of differentiation

A

keratinocytes

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9
Q

___________ __________ have defensins and these are secreted into the waterproof lipid layer of the skin

A

Lamellar bodies

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10
Q

The lungs have bronchial __________ epithelium. What does this have to do with immunity?

A

ciliated

Airways lined by cilia. Beating moves stream of mucus secreted by goblet cells

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11
Q

The gut epithelium contains ______ cells that are deep in the epithelial crypts and produce antimicrobial defensins + the lectin RegIII

A

Paneth

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12
Q

Reg III proteins belong to the family of ____-type lectin regenerating islet-derived proteins.

A

C

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13
Q

The RegIII (regenerating gene family protein III) lectins belong to the antimicrobial proteins, and are expressed in epithelial cells of the…

A

stomach, small intestine and colon

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14
Q

The RegIII (regenerating gene family protein III) lectins belong to the antimicrobial proteins, and are expressed in epithelial cells of stomach, small intestine and colon. Subsequently, they are secreted into the….

A

gut lumen

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15
Q

RegIIIβ binds peptidoglycan and lipid A respectively, and thus can kill certain _________________ and ______________ bacteria, including the gut commensal microbiota and enteropathogenic bacteria.

A

Gram-positive and Gram-negative

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16
Q

What does lysozyme do and where is it found?

A

contains a glycosidase enzyme that breaks down bonds in peptidoglycan

found in tears, saliva, and Paneth cells

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17
Q

What are the 4 types of antimicrobial peptides?

A

1) defensins
2) cathelicidins
3) histatins
4) lectin

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18
Q

Defensins are ________ conserved in eukaryotic organisms

A

highly

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19
Q

What are defensins?

A

antimicrobial peptide

short cationic peptides w/ 3 disulfide bonds and a pos. charges region separated by hydrophobic areas

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20
Q

Do cathelicidins contain disulfide bonds?

A

no

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21
Q

Who carries cathelicidin genes?

A

mice and humans

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22
Q

Who makes cathelicidins? For what purpose?

A

by neutrophils and macrophages

made in response to infection in keratinocytes and epithelial cells in lungs/intestine

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23
Q

Histatins are constitutively produced in ________ ________ by parorid, sublingual, and submandibular glands.

A

oral cavity

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24
Q

Histatins are _______ against pathogenic fungi and wound healing in oral cavity

A

active

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25
Q

What is lectin? What is an ex?

A

antimicrobial peptide

Bactericidal carbohydrate binding protein made by epithelial cells

Ex: Reg3 is made by Paneth cells and works better on G plus cells by making hole in membrane

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26
Q

Defensins, cathelicidins, and histatins are activated by _______________ to release an amphipathic antimicrobial peptide

A

proteolysis

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27
Q

Electrostatic attraction and the transmembrane electric field brings the defensins into the lipid bilayer. What does defensin do?

A

defensin peptides form a pore

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28
Q

What are the 2 types of bacteria?

A

1) gram-positive bacteria
2) gram-negative bacteria

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29
Q

What is the difference between gram pos and gram neg bacteria?

A

gram pos has a much thicker peptidoglycan wall

gram neg contains LPS and an additional outer membrane, peptidoglycan is thinner than gram pos

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30
Q

______________ or ______________ have to get through the peptidoglycan wall to expose the lipid bilayer

A

Lysosomes or defensins

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31
Q

The complement system is made up of 30+ proteins produced by the _________

A

liver

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32
Q

complement proteins circulate around the body in their _______ form

A

inactive

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33
Q

In the presence of pathogens or Ab bound to pathogen, the ____________ system will be activated

A

complement

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34
Q

What are the final outcomes of the complement system?

A

kill pathogen, phagocytose it, inflammation to fight off
infection

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35
Q

What are the stages of complement action?

A
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36
Q

What complement proteins are there (C___-C____)?

A

C1-C9

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37
Q

Simplest terms, what does C1q do?

A

bind Ab

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38
Q

Simplest terms, what does C4b and C3b do?

A

bind surface

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39
Q

What are the inflammatory mediator complement proteins?

A

C5a, C3a, C4a

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40
Q

What are the MAC complement proteins?

A

C5b, C6-C9

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41
Q

What do the regulator complement proteins do?

A

they regulate immune system and don’t activate the complement system/inflammatory response unless they absolutely have to

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42
Q

The complement system recognizes features of microbial surfaces and marks them for destruction by coating them with _____

A

C3b

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43
Q

Complement activation is largely confined to the
surface on which it is ________

A

initiated

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44
Q

What are the 3 pathways in innate immunity?

A

1) classical
2) alternative
3) mannose binding lectin (MBL) pathway

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45
Q

The lectin pathway, or mannose-binding lectin (MBL) and ficolins recognize and bind ________ on pathogen surface

A

carbohydrates

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46
Q

Classical pathway has _____ that interacts with pathogen surface or with antibodies bound to the surface

A

C1q

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47
Q

Alternative pathway has ____ that undergoes spontaneous hydrolysis to C3(H2) to initiate eventual deposition of C3 convertase on microbial surfaces

A

C3

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48
Q

All 3 pathways generate a _____ convertase, which cleaves C3, leaving C3b bound to the microbial surfaces and releasing C3a

A

C3

this is a crucial step!! no turning back now

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49
Q

What is the goal of all 3 pathways?

A

make C3 convertase and have it split to C3a and C3b

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50
Q

After all 3 pathways generate a C3 convertase, C3a and C__a recruit phagocytic cells to the site of infection and promote inflammation

A

C5a

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51
Q

After all 3 pathways generate a C3 convertase, phagocytes with receptors for ____ engulf and destroy the pathogen

A

C3b

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52
Q

After all 3 pathways generate a C3 convertase, completion of the complement cascade leads to the formation of a ________________, which disrupts cell membrane and causes cell lysis

A

membrane attack complex (MAC)

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53
Q

C3b forms a covalent bond with the microbial surface. Covalent bond is possible due to a….

A

thioester domain (TED) hidden inside folded C3 protein

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54
Q

When C3 is cleaved (opening up the bond), the thioester domain can react with nearby ________ or ________ group on microbial surface

A

hydroxyl or amino

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55
Q

The newly synthesized C3 protein is cleaved to generate a _______ chain and an ________ chain held together by disulfide bonds

A

beta, alpha

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56
Q

Before cleavage of C3 convertase, the ____________ bond within TED is protected from reacting.

A

thioester

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57
Q

Cleavage of C3 releases ____ and a change in conformation of ______ allows the thioester bond to react with a chemical group on the pathogen surface

A

C3a, C3b

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58
Q

The reactive thioester group of C3b is in TED. What happens now?

A

C3b is bound to pathogen surface (tags the pathogen)

or

C3b can be inactivated by hydrolysis

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59
Q

The classical pathway is initiated by activation of the ______________

A

C1 complex

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60
Q

C1 is a pathogen sensor and interacts directly with
pathogen and with __________ that are bound to
pathogens.

A

antibodies

61
Q

Can C1 work in both innate and adaptive immune system?

A

YES

62
Q

What is the function of C1q in the classical pathway?

A

binds directly to pathogen surfaces or indirectly to antibody bound to pathogens, thus allowing autoactivation of C1r

63
Q

What is the function of C1r in the classical pathway?

A

cleaves C1s to active protease

64
Q

What is the function of C1s in the classical pathway?

A

cleaves C4 and C2

65
Q

What is the function of C4b in the classical pathway?

A

covalently binds to pathogen and opsonizes it. Binds C2 for cleavage by C1s

66
Q

What is the function of C2a in the classical pathway?

A

active enzyme of classical pathway C3/C5 convertase and also cleaves C3 and C5

67
Q

What are the functions of C3b in the classical pathway?

A

-binds to pathogen surface and acts as opsonin
-initiates amplification via the alternative pathway
-peptide mediator of inflammation (immediate activity)

68
Q

What is the first step of the complement system classical (antibody dependent) pathway?

A

soluble antibody binds to a soluble antigen or to an antigen associated w/ a bacterial cell (IgG or IgM primarily)

69
Q

What is the 2nd step of the complement system classical (antibody dependent) pathway?

A

binding induces changes in the antibody Fc portion
-exposes a binding site for the C1 protein
>C1 is a complex of 1q, 2r, and 2s subunits (C1= C1qr2s2)
>q forms a stalk w/ branches, r/s binds to branches
-binding of C1 to antibody requires multiple Fc to be in close proximity (IgM)

70
Q

What is the 3rd step of the complement system classical (antibody dependent) pathway?

A

binding to the antibody activates C1r to cleave C1s (now have active C1s)

(Ab on pathogen, C1 binds to it)

71
Q

What is the 4th step of the complement system classical (antibody dependent) pathway?

A

C4 binds to C1s and is converted into an active C4b fragment and smaller C4a fragment
-C4b attaches to target surface near the Ab

72
Q

What is the 5th step of the complement system classical (antibody dependent) pathway?

A

at the same time as step 4, C2 is cleaved by C1s into a larger C2a and smaller C2b

73
Q

In the complement system classical (antibody dependent) pathway, C1 binds and will be converted to an active fragment and then cleave C4. What does this generate/what happens?

A

-generates C4a and C4b
-C4b will land on surface of agent
-C4 cleavage will also bring out cleavage of C2

74
Q

What is the 6th step of the complement system classical (antibody dependent) pathway?

A

the C4b and C2a form a complex (C4b2a is also called C3 CONVERTASE)

75
Q

What is the 7th step of the complement system classical (antibody dependent) pathway?

A

C3 convertase converts a large number of C3 into C3a (small) and C3b (large enzyme)

76
Q

What is the 8th step of the complement system classical (antibody dependent) pathway?

A

some of the C3b produced combines w/ C4b2a ro form C4b2a3b (called C5 convertase)
-some of the C3b does other things

77
Q

What is the 9th step of the complement system classical (antibody dependent) pathway?

A

C5 convertase binds to C5 and cuts it into C5b (large) and C5a (small)
-C5b produced will initiate later steps!

78
Q

The lectin pathway uses soluble receptors that recognize microbial surfaces (_____________________________) to activate the complement cascade.

A

LPS, glycans on yeast surface

79
Q

What sugar is more abundant in foreign agents like bacteria and yeast, as opposed to humans? What do humans have that is more abundant?

A

mannose sugar

humans are abundant w/ sialic acid

80
Q

Mannose binding lectins (MBL) is made in the ________

A

liver

81
Q

MBL assembles into _________ that float in blood. What happens in this form?

A

trimers

When in trimer form have high affinity for glycans on bacteria. Low affinity for sialic acid ends

82
Q

Ficolins are found in various tissues and are a group of proteins containing both a __________-like and a __________-like domain.

A

collagen, fibrinogen

83
Q

Where are ficolins secreted?

A

in the liver

84
Q

What does ficolins have a high and low affinity for?

A

High affinity for oligosaccharides with acetylated
sugars on bacteria.

Low affinity for mannose containing sugars

85
Q

MBL monomers form trimeric clusters of ______________ domains. MBL binds w/ high affinity to mannose and fucose residues

A

carbohydrate-recognition

86
Q

Ficolins are similar in structure to MBL but have a different carbohydrate-binding domain. What do they bind to?

A

oligosaccharides containing acetylated sugars

87
Q

MBL forms complex with MBL associated _________ _____________ (MASP) which are inactive

A

serine proteases

88
Q

When MBL binds to pathogen surface, conformational change in MASP 1 allows it to activate _______

A

MASP 2.

89
Q

MASP 2 cleaves C2 and C4. C4 also has buried ________ bond. C4a is released and C4b has a conformational change. The ________ bond is accessible to bind to the microbial surface. It bind with C2 on surface. Now this cleaves C3 into C3a and b. C3a is released and inflammatory response begins. C3b on the surface can be opsonized

A

thioester, thioester

90
Q

Activated MASP-2 associated w/ MBL or ficolin cleaves C4 to C4a and C4b, which binds to the microbial surface. What happens next?

A

-C4b then binds to C2, which can then be cleaved by MASP2 to C2a, with which it forms the C4b2a complex and C2b
-C4b2a is an active C3 convertase cleaving C3 to C3a and C3b, which binds to the microbial surface or to the convertase itself
-one molecule of C4b2a can cleave up to 1000 molecules of C3 to C3b. Many C3b molecules bind to the microbial surface

91
Q

What is the first step of the complement system alternative (antibody independent, no antibody required) pathway?

A

activation=
-occurs when C3b (produced as a result of slow constant hydrolysis) binds to a foreign surface Ag

92
Q

What is the 2nd step of the complement system alternative (antibody independent, no antibody required) pathway?

A

C3b bound to the surface binds to another serum protein Factor B (floating around in blood)
-binding alters structure B and makes it accessible to be cut by the protein Factor D

93
Q

What is the 3rd step of the complement system alternative (antibody independent, no antibody required) pathway?

A

the resulting complex C3bBb acts as a C3 convertase and produces a lot more C3b
-some of that binds to C3bBb and forms C3bBbC3b

94
Q

What is the 4th step of the complement system alternative (antibody independent, no antibody required) pathway?

A

C3bBbC3b acts as a C5 convertase –> C5b is produced

95
Q

The alternative pathway is an amplification loop for C3b
formation that is accelerated by ___________ in the presence of pathogens.

A

properdin

96
Q

C3b is deposited by the classical pathway or lectin pathway C3 convertase. What happens next for alternative pathway?

A

-C3b binds to Factor B
-Bound factor B is cleaved by plasma protease Factor D into Ba and Bb
-C3bBb complex is a C3 convertase, cleaving many C3 molecules to C3a and C3b

97
Q

Factor B contains a serine protease (SP) domain, and when activated it provides the catalytic activity of the _______________ pathway C3 and C5 convertases. Factor B circulates as an inactive proenzyme (i.e., a zymogen), and only becomes activated after cleavage by the protein factor D. However, factor D can only cleave factor B when it is bound to the active forms of C3:
C3(H2O) and C3b. Factor B is generated as a single-chain protein, and cleavage by factor D generates two peptide fragments (Ba and Bb).

A

alternative

98
Q

Factor D is a serine protease (SP) consisting of a single polypeptide of 228 amino acids. Unlike other SPs in the complement system, factor D circulates in the plasma as a mature but ‘resting-state’ form at a very low concentration and is produced mainly
in _________________

A

adipocytes.

99
Q

In the alternative pathway, C3 undergoes spontaneous hydrolysis to C3(h2O), which binds to factor B, allowing it to be cleaved by factor D into Ba and Bb. What happens next?

A

-the C3(h2O)Bb complex is a C3 convertase, cleaving more C3 into C3a and C3b. C3b is rapidly inactivated unless it binds to a cell surface
-Factor B binds noncovalently to C3b on a cell surface and is cleaved to Bb by factor D

100
Q

What is the function of C3b in the alternative pathway?

A

-binds to pathogen surface
-binds factor B for cleavage by factor D
-C3bBb is a C3 convertase and C3b2Bb is a C5 convertase

101
Q

What is the function of Bb in the alternative pathway?

A

Bb is the active enzyme of the C3 convertase C3bBb and the C5 convertase C3b2Bb

102
Q

What is the function of Factor D in the alternative pathway?

A

plasma serine protease, cleaves Factor B when it is bound to C3b to Ba and Bb

103
Q

What is the function of properdin (P) in the alternative pathway?

A

plasma protein that binds to bacterial surfaces and stabilizes the C3bBb convertase

104
Q

C3 convertase is unstable, why?

A

bc you want it to cleave quickly

105
Q

Is C3 convertase short lived or long lived?

A

short lived

106
Q

What is C3 convertase stabilized with?

A

stabilized by binding the plasma protein Properdin
(Factor P)

107
Q

______________ is made by neutrophils and
stored in granules

A

Factor P

108
Q

Factor P may do _____________ ____________
on pathogens and is released

A

pattern recognition

109
Q

Properdin (Factor P) binds to bacterial surface and helps bring about _____________ activity

A

complement

110
Q

Pathogens lack _________________ proteins. Binding of properdin (factor P) stabilizes the C3bBb complex. What happens next?

A

complement-regulatory

-C3bBb complex is a C3 convertase and deposits many molecules of C3b on the pathogen surface
-opsonization, activation of terminal components

111
Q

Surface-bound C3 convertase deposits large
numbers of C3b fragments on pathogen surfaces and
generates _____ __________ activity. Some of the C3b produced combines with C4b2a to form C4b2a3b (called C5 convertase) in the alternative pathway

A

C5 convertase

112
Q

C5 convertase binds to C5 and cuts it into C5b (_______)
and C5a (_______)

A

large, small

113
Q

C3b binds to both C4b2a and C3bBb, forming the active C5 convertases C4b2a3b and C3b2Bb. What happens next?

A

-C5 binds to the C3b component of the C5 convertase enzyme
-C5 is cleaved by C2a or Bb to form C5b and C5a

114
Q

End result of activating all three complement pathways is the formation of _______

A

C5b

115
Q

End result of activating all three pathways is the formation of C5b. So what happens now?

A

-After being produced, C5b (acts like a recruiter) binds to the surface of the target
>It will serve as a docking site for the rest of the components of the MAC
-C5b on the surface is unstable
>Must be stabilized by the binding of C6
-When C7 binds to C5bC6, the trimeric complex undergoes a conformational change which exposes a hydrophobic region of the protein
>Allows it to insert itself into the phospholipid bilayer
-C8 binds to C5bC6C7 and together form a small pore in the membrane
-The C5bC6C7C8 complex serves as docking site for binding of a perforin-like protein called C9 (polymerizes and increases size of the pore–> cell dies)

116
Q

Membrane and plasma proteins that regulate the formation and stability of C3 convertases
determine the extent of…

A

complement activation.

117
Q

Many reg. proteins present in plasma to protect host cells. These proteins interact with C3b and prevent the convertase from forming or cause its rapid _____________

A

disassociation

118
Q

Inactivation can happen from cleaving C3b. Plasma protein ___________ can do this by binding to C3b. Factor H also binds C3b (preferentially on sialic acid which is in vertebrates) and inactivates it.

A

Factor I

119
Q

What 2 plasma proteins ensure that C3 does not get activated?

A

Factor I and Factor H

120
Q

T/F:

Complement can attack both the pathogen and the infected host under the right conditions

A

true!

this must be strictly regulated to minimize abnormal activation

121
Q

What are the 2 main mechanisms of complement regulation?

A

1) Overall instability of complement intermediates
2) Inhibitory proteins

122
Q

One of the mechanism of complement regulation is overall instability of complement intermediates. What does this mean?

A

-Most components degrade quickly if not stabilized by other components
-If one gets activated abnormally, it typically gets degraded within a few min
-Example: C3b produced must bind to C3 convertase immediately or be degraded

123
Q

One of the mechanisms of complement regulation is inhibitory proteins. List the inhibitory proteins

A

(Wide variety – can affect different steps in different pathways)

A) Inhibitor of C1 (only classical affected)
B) Inhibitors of C3 convertase
C) Inhibitors of the MAC

124
Q

Who is the inhibitor of C1? What pathway is affected and what does it do?

A

Called C1 inhibitor (C1inh)

only affects classical pathway

binds to C1 and causes C1r2s2 to come off of C1q

125
Q

Why are the inhibitors of C3 convertase important?

A

C3 convertase is the major point of amplification in all 3 pathways

Tons of C3b is made by this enzyme –> can create great damage

126
Q

Talk about the inhibitors that block the classical/lectin C3 convertase

A

-Some bind to C4b and prevents its association with C2a and others (DAF) actively dissociate it when it forms
-Another (Factor I) binds to C4b and destroys it

127
Q

Talk about the inhibitors that block the alternative C3 convertase

A

-Bind to C3b and prevent association with Factor B
-Some also cut C3b, destroying it (Factor I)

128
Q

Talk about the inhibitors of the MAC

A

-Some block C5b67 from inserting into the membrane (S protein)
>Prevents it from coming out from 1 cell and inserting into an innocent bystander cell
-Others block C9 from associating with C5b678 (blocks self cell destruction)

129
Q

Pathogens produce several types of proteins that can __________ complement activation

A

inhibit

130
Q

Complement activation can lead to cell lysis, inflammation, opsonization, and _____________ of immune complexes

A

clearance

131
Q

What happens with the lysis of cells by the MAC?

A

The MAC is capable of destroying Gram-negative bacteria, enveloped viruses, parasites, RBCs, and nucleated cells (can be activated by antibody or microbial products)

132
Q

What are some examples of resistance mechanisms?

A

1) Gram neg bacteria–> some produce extra polysacc in their LPS, this prevents MAC from inserting into the inner membrane
2) Gram pos bacteria –> almost always totally resistant bc of their thick peptidoglycan layer prevents MAC from insertion into the membrane
3) many pathogens produce inhibitors to complement proteins
4) cancer cells can engulf the MAC before it can kill

133
Q

Many of the smaller _____ fragments produced by complement protein cleavage help to induce an inflammatory response. These proteins are called anaphylatoxins. What are the 3 main ones?

A

(a)

C3a, 4a, and 5a

134
Q

What are the 5 functions of anaphylatoxins?

A

1) Bind to receptors on basophils and mast cells and trigger degranulation (release of pro-inflammatory chemicals)
2) Induce smooth muscle contraction and increased vascular permeability
3) Promote increased leukocyte adhesion (to vessel walls) and extravasation
4) Serve as a chemoattractant for movement of immune cells through the tissue
5) Stimulate respiratory burst in neutrophils

135
Q

What is respiratory burst?

A

increase in oxygen consumption to increase energy in cells

136
Q

___ is a great opsonin. What does it do?

A

C3b

binds to the surface of the Ag and tags it for destruction by phagocytes

137
Q

Most phagocytes have ______________ receptors

A

complement

138
Q

The repeating nature of most viral structural components (e.g. capsids) stimulates complement activation…..

A

w/ or w/o antibody

139
Q

Complement proteins can neutralize virions in several different ways. What are they?

A

1) C3b coats the surface (w/ Ab) and causes them to aggregate
-Instead of having 1,000 individual infectious particles, have 1 large aggregate
2) Prevents viral particles from binding to receptors on target cells
3) They are opsonized and targeted for destruction by phagocytes (CR1)
4) MAC can punch holes in the membrane of enveloped viruses

140
Q

Some viruses have developed mechanisms of evading the complement system. Give an example

A

1) Herpesviruses produce a fake FC receptor (locks up all the Ab)
2) Vaccinia virus produces proteins that directly inhibit complement proteins

141
Q

How does the immune system dispose of complexes containing antibodies and small, soluble antigens from our blood?

A

-Fc receptors on phagocytes play some role
-Complement plays a more important role

142
Q

What are the general steps for the clearance of immune complexes via complement?

A

1) C3b can bind to antibodies that have bound soluble antigen into a complex
2) The C3b then binds to CR1 on the surface of a RBC
3) RBC circulates and ends up at the liver and spleen
-Complexes are stripped off their surface and immediately get degraded by local phagocytes

Note: tons of RBCs in our blood, few phagocytes

143
Q

_____________ of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins.

A

Ingestion

144
Q

Bacterium is coated w/ C3b. What now?

A

-when only C3b binds to CR1, bacteria will not be able to undergo phagocytosis
-C5a needs to also bind to activate macrophages to phagocytize via CR1 (C5a binds to a GPCR on the surface)

145
Q

What are some defects in regulators?

A

-Factor I deficiency leads to uncontrolled complement activation, complement proteins become depleted
and people suffer from repeated bacterial infections.
-Single nucleotide polymorphisms in factor H gene, is related age-related macular degeneration; leading
cause of blindness in the elderly in developed countries.

146
Q

Mutations in central players such as ______ and ______ can lead to more severe problems

A

C3 and C5

147
Q

Diseases can be subdivided into 4 groups. What are they?

A

1) Those that result from inefficient cell lysis
2) Those that result from poor opsonization
3) Those that result from poor clearance of immune complexes
4) Those that result from inefficient regulation of inflammation

148
Q

Recurrent bacterial and fungal infections can lead to what?

A

major increases in Staph, Strep, and Neisseria infections

149
Q

What can a hyperactive inflammatory response lead to?

A

-Too many immune complexes floating around (or too many anaphylatoxins) can lead to the continual activation of the inflammatory response
-Can lead to lupus, chronic kidney inflammation, vasculitis

Immuno (7 decks)

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