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path300 > Immune diseases > Flashcards

Immune diseases Flashcards

1
Q

what cells produce mucus?

A

goblet cells

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2
Q

what cells secrete antimicrobial peptides?

A

Paneth cells

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3
Q

what are the components of MAC?

A

C5b, C6, C7, C8, C9

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4
Q

which complement component is recognized by phagocytes? (opsin)

A

C3b

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5
Q

which complement components act as chemotactic agents?

A

C3a, C4a, C5a

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6
Q

what is the link of complement with antibodies?

A

they can form functional complexes with antibodies to facilitate the clearance of antigens by phagocytes

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7
Q

name the types of innate immune cells

A

mast cells, neutrophils, macrophages, DCs

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8
Q

what do Fc receptors recognize?

A

antibodies

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9
Q

what is special about PAMPs?

A

they are essential for the viability of the microbes and cant be mutated

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10
Q

what other than PAMPs can PRRs recognize?

A

flagella on bacteria, nucleic acid on viruses, GPI anchor on parasites

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11
Q

where can PRRs be found?

A

innate immune cells and epithelial cells

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12
Q

what does activation of PRRs lead to?

A

production of cytokines and chemokines that help recruit other immune cells

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13
Q

what do mast cells recognize? with what receptor? leads to what?

A

IgE antibodies with Fc receptors; activation

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14
Q

2 ways how mast cells help immune response?

A
  1. degranulation -> release histamine, proteases, chemotactic factors
  2. metabolism of membrane phospholipids (arachidonic acids -> prostaglandins + leukotrienes) -> sm contraction and vasodilation
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15
Q

what are mast cells involved in?

A

type I hypersensitivity (allergic) reaction, neutrophils extravasation, vasodilation

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16
Q

what process do neutrophils go through to participate in the immune response?

A

extravasation

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17
Q

where can we find neutrophils?

A

in circulation

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18
Q

what type of agents do neutrophils produce?

A

antimicrobial agents: ROS, cathepsin G, defensins

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19
Q

what happens if NETs are not cleared up rapidly?

A

they persist and result in cell damage through enhanced inflammatory processes

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20
Q

where are innate cell macrophages found?

A

in tissue

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21
Q

where are tissue-resident vs monocyte-derived macrophages from?

A

tissue-resident macrophages are derived from yold sac or fetal liver.
monocyte-derived macrophages are derived from bone marrow.

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22
Q

what 6 different tasks can macrophages perform?

A

antimicrobial actions through ROS.
antigen presentation.
antigen/antibody uptake.
wound healing through GF production.
phagocytosis.
bone resorption through osteoclasts.

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23
Q

what are DCs cell called in the skin?

A

Langerhans cells

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24
Q

what cells do DCs arise from?

A

monocytes

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25
Q

what is the most efficient APC?

A

dendritic cell

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26
Q

what are the structure of MHC class 1 and II molecules?

A

MHc class I = alpha chain + variant beta macroglobulin chain
MHC class II = alpha + beta chain

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27
Q

what are MHC called in humans? where is the gene located?

A

HLA;
chromosome 6

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28
Q

everyone has different HLA genes except?

A

except identical twins

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29
Q

what is the only cell that can activate naive T cells?

A

dendritic cell

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30
Q

where do innate lymphoid cells originate from?

A

hematopoietic stem cells in bone marrow

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31
Q

name the innate and adaptive immune cells from each lineage

A

innate myeloid lineage: neutrophil, eosinophil, basophil, monocyte, macrophage, dendritic cells, mast cells, platelets
adaptive lymphoid lineage: t cells and b cells

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32
Q

what is special about NK cells origin

A

derived from lymphoid progenitor but are innate immune cells

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33
Q

what are the 2 ways how NK cells kill?

A
  1. induce apoptosis by producing perforins and granzyme proteins.
  2. Fas ligand triggers cell death
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34
Q

what can tumor cells downregulate to evade immune regulation? what does this downregulation trigger regarding NK cells?

A

downregulate MHC class I. decreases the inhibitory signal that the NK cells recives -> activates NK cell -> kill

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35
Q

what does each of the 3 classes of innate lymphoid cells respond to?

A

ILC1: intracellular pathogens
ILC2: parasites
ILC3: extracellular bacteria and fungi

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36
Q

how is the variable regions of TCR generated? what does this allow for?

A

from VDJ recombination.
allows for specificity

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37
Q

where do t and b cells differentiate and mature?

A

both differentiate in bone marrow.
T cells mature in the thymus (become CD4/8 +)
B cells finishes maturation in lymph nodes

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38
Q

name the different subtypes into which CD4+ t cells can further differentiate in peripheral tissue, and their associated cytokine

A

TH2 cells: produce IL-4. involved in allergies
TH1 cells: produce IFNy
TH17 cells: produce IL-17 (TH1 and TH17 are involved in type IV hypersensitivity and autoimmune diseases)
Treg: TGFB

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39
Q

what happens in the lymph node to complete the maturation of B cells?

A

b cells enter through afferent lymphatic vessels, proliferate in primary follicles, become germinal centers when in contact with antigen. they fully mature and become plasma cells and exit through efferent lymphatic vessels

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40
Q

2 ways how B cell can activate

A
  1. T cell-independent: recognize antigen and BCRs aggregate
  2. T cell-dependent: through cytokines
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41
Q

antibody receptor produced by naive B cells

A

IgM receptors

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42
Q

what enzyme helps with variable region hypermutation of IgM receptors?

A

AID enzyme (activation-induced cytidine deaminase)

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43
Q

what antibodies do plasma cells secrete at a distance?

A

IgM or IgG

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44
Q

what are antibodies effector functions?

A

Neutralization of microbes and toxins.
Opsonization and phagocytosis of microbes recognized through Fc or C3b receptors.
Antibody-dependent cellular toxicity: activation of NK cells.
Complement activation to facilitate inflammation and lysis of microbes.

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45
Q

3 types of immune system failures

A

hypersensitivity, autoimmunity, immunodeficiency

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46
Q

what are the 4 types of hypersensitivity reactions? describe

A

type I: immediate T cell dependent allergic reaction
type II: antibody specifically recognizes a receptor on cell surface
type III: antibody driven: immune complexes trigger neutrophils activation and inflammation
type IV: delayed t cell dependent reaction involving TH1 and TH17

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47
Q

which cells and cytokines are involved in type I hypersensitivity?

A

Th2 cells and IL4, IL5, IL13, IGe production

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48
Q

what are the 2 steps of type I hypersensitivity reaction (during secondary exposure)?

A
  1. initial response within minutes & mast cells activation
  2. late phase reaction: cytokines infiltration other cell types
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49
Q

what do mast cells do after the second exposure to allergen (Type I hypersensitivity)

A

degranulate and release histamine

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50
Q

features of the secondary exposure of type I hypersensitivity?

A

mast cells, vasodilation, pain, eosinophils recruitment, hyperactive mucous production, platelets activation

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51
Q

what are the clinical manifestations of Type I reaction?

A

hay fever, food allergies
bronchial asthma

52
Q

describe bronchial asthma

A

repeated exposure to antigen causing massive tissue remodeling. treated by bronchodilators

53
Q

what can cause a systemic type I hypersensitivity reaction?

A

snake venom, food allergies

54
Q

what do chemical mediators released during type I hypersensitivity reaction cause?

A

constriction of airways, GI tract dysfunction, diarrhea, massive drop in BP

55
Q

what parasite did Th2 response evolve to deal with?

A

helminth

56
Q

different mechanisms of type II hypersensitivity

A

phagocytosis, inflammation (complement system), blocking receptor function

57
Q

what disease is associated with type II hypersensitivity blockage of receptor function?

A

Grave’s disease due to overproduction of hormones by thyroid epithelial cells

58
Q

explain newborn hemolytic anemia

A

1st child has a different blood type than mother -> mother produces antibodies at birth -> second child also has different blood type -> attack the baby’s RBCs

59
Q

what is the main feature of type III hypersensitivity reaction?

A

immune complex deposition made of antigens and antibodies aggregation

60
Q

what do immune complexes cause in type III hypersensitivity?

A

complement activation, recruitment of granulocytes that cause release of proteases and oxygen free radicals = tissue damage

61
Q

what is diphteria? what animal is naturally immune and can raise antibodies?

A

serum sickness; upper respiratory tract bacterial infection.
example of type III hypersensitivity.
Horse

62
Q

what is glomerulonephritis?

A

immune complexes accumulate in glomerulus in kidneys + immune cell proliferation.
can cause renal failure.
type III hypersensitivity reaction.

63
Q

differences between type II and II hypersensitivity?

A

type II: Antibody-Antigen interaction takes place on the cell surface of the target cell (bumpy immunofluorescence)
type III: Antibody-Antigen interaction forms free-floating complexes that can precipitate on tissues (linear immunofluorescence)

64
Q

what 2 types of reactions are included in type IV hypersensitivity?

A
  1. delayed-type hypersensitivity: CD4+ T cells release cytokines
  2. CD8+ T cell-mediated cytotoxicity: CD8+ T cells directly kill their target cell
65
Q

what cell type will naive CD4+ t cells differentiate into with type IV hypersensitivity? what do they release

A

Th1: releases IFN-y for macrophages differentiation
and Th17: recruit neutrophils via IL-6

66
Q

what is a delayed-type hypersensitivity reactions? name an example and describe both phases

A

poison ivy.
Sensitization phase: hapten (in this case urushiol) gets absorbed by the dermis, picked up by langerhans cells, activation of CD4+ T cells -> IL-12 -> Th17 and Th1 differentiation
Effector phase: granulocytes secrete granules, causing tissue damage. Th1 releases INF-y and activates macrophages -> pro-inflammatory cytokines -> tissue damage

67
Q

why is the tuberculin test necessary?

A

Tuberculosis is often present in the latent form, so need to test for past exposure

68
Q

what can delayed type IV hypersensitivity create? why

A

granulomas; continual activation of macrophages

69
Q

how do CD8+ t cells kill target cells?

A

release granzymes and perforin -> apoptosis of target cell

70
Q

give 2 examples of CD8+ t cell-mediated toxicity type IV hypersensitivity

A

graft rejection and type I diabetes

71
Q

what happens in type I diabetes?

A

autoimmune reaction against beta cells mediated by CD8+ T cellls

72
Q

which cells delete the self-reactive t cells? where?

A

T reg in the thymus

73
Q

what is anergy (related to lymphoid cells)

A

B and T cells failing to respond

74
Q

name 4 autoimmune diseases

A

lupus, multiple sclerosis, Crohn’s disease, rheumatoid arthritis

75
Q

genes encoding for what could be involved in autoimmune diseases

A

HLA, PTPN22 (immune cell activation), cytokine signaling, autophagy

76
Q

what can microbe infection do to co-stimulation, causing autoimmune disease?

A

upregulation of co-stimulatory molecules on APCs, increasing self-reactive T cells

77
Q

what is molecular mimicry?

A

APCs present microbial peptides that resemble self-antigen to T cells, which activates T cells against self-tissue

78
Q

who is more affected by autoimmune diseases?

A

women because we have enhanced immunity & estrogen may be pro-inflammatory & X-linked genes encode immmunity

79
Q

what is RA?

A

Rheumatoid Arthitis: chronic inflammation in the joints; symmetrical;
leads to joint deformity and disability

80
Q

where other than joints can RA have effects?

A

nodules, lung, eyes, vasculitis

81
Q

what are rheumatoid factors?

A

anti-IgG auto-antibodies (anti-citrullinated protein antibodies ACPC) & IgM antibodies that bind to self-IgG

82
Q

what are the hypothesized causes of RA?

A

genetics (HLA subtype genes)
predisposing environmental triggers (smoking, infection) causing post translational modifications

83
Q

what type of hypersensitivity is autoimmune disease?

A

type III

84
Q

what are PAD and what do they do?

A

peptidylarginine deiminase: converts arginine to citrulline -> immune system now responds to protein

85
Q

what other modifications can cause self-reaction?

A

carbamylation (irreversible), IgG antibody glycation

86
Q

how can RA be detected?

A

presence of anti-citrullinated proteins aantibodies in blood.
X ray for erosion.
Rheumatoid factors.

87
Q

what are characteristics of osteoarthritis joints?
vs of Rheumatoid joints?

A

osteoarthritis: bone erosion from rubbing leading to inflammation.
Rheumatoid: inflammation in synovial space

88
Q

what causes synovial inflammation in RA?

A

macrophages, DCs, lymphocytes, plasma cells infiltrate synovial space and attack the cells causing hyperplastic synovium (pannus); fibroblast and myoblasts within the membrane because highly proliferative

89
Q

name inflammatory mediators in RA

A

INF-y, IL-17, TNF, IL-1, RANKL (promotes osteoclasts)

90
Q

what are symptoms of systemic lupus erythematosus?

A

butterfly rash, hair loss, swollen joints, light sensitivity

91
Q

what causes SLE (systemic lupus erythematosus)

A

clearance failure of debris (ex NETs) by immune system -> autoimmunity

92
Q

what is the main characteristic of SLE systemic lupus erythematosus

A

production of autoantibodies, triggering a type III OR type II hypersensitivity reaction

93
Q

how does glomerulonephritis occur in SLE?

A

due to deposition of autoantibodies in the vasculature of the glomerulus

94
Q

what cell types are affected by MS?

A

CNS: oligodendrocytes (attacks myelin sheaths)

95
Q

what are characteristic of MS?

A

plaque formation & fibrosis, defects in conductivity

96
Q

how does MS happen?

A

leaky blood-brain barrier & integrin expression -> T cells enter brain and interact with microglia -> cytokine release, macrophages activation -> myelin is attacked

97
Q

what are the root causes of MS?

A
  • genetics: class I and class II MHC genes (ex HLA-DR2)
  • vitamin D deficiency
  • viral infections: EBV latency antigen
98
Q

describe the 4 types of MS (course of the disease)

A

relapsing-remitting: unpredictable attacks
primary progressive: steady increase
secondary progressive: attacks followed by steady increase
progressive-relapsing: steady increase with attacks

99
Q

broadly describe the 2 types of IBD

A

Crohn’s disease: lesions (transmural inflammation, ulceration, fissures) in GI tract and granulomas formation
Ulcerative colitis: ulcers in distal colon causing pseudo-polyps

100
Q

is Crohn’s disease an autoimmune disease?

A

no! immune-related process

101
Q

what mutations and environmental factors can cause Crohn’s disease?

A

mutations = NOD2: innate immune receptor that senses GI tract microbiome
env = reduced microbial diversity

102
Q

what can cause ulcerative colitis?

A

molecular mimicry/cross reactivity of perinuclear anti-neutrophil cytoplasmic antibodies pANCA

103
Q

what can cause ulcerative colitis?

A

molecular mimicry/cross reactivity of perinuclear anti-neutrophil cytoplasmic antibodies pANCA

104
Q

describe the 2 causes of graft rejection?

A
  • mismatch MHC molecules: direct or indirect (involves MHC uptake by APC)
  • mismatch MiHA genes: short segments that are very variable between people
105
Q

describe the 3 types of host vs graft rejection

A
  • hyperacute: immediate onset; caused by blood type incompatibility, preformed antibodies react to donor tissue and cause thrombosis and occlusion
  • acute: weeks to months; T-cell mediated; leukocyte infiltration of graft vessels
  • chronic: months to years; causes thickening and fibrosis of graft vessels
106
Q

describe the 3 types of host vs graft rejection

A
  • hyperacute: immediate onset; caused by blood type incompatibility, preformed antibodies react to donor tissue and cause thrombosis and occlusion
  • acute: weeks to months; T-cell mediated; leukocyte infiltration of graft vessels
  • chronic: months to years; causes thickening and fibrosis of graft vessels
107
Q

where does graft vs host disease happen?

A

skin, liver, intestine

108
Q

why does graft vs host disease happen?

A

immunocompetent tissue is transplanted into an immunocompromised host -> graft T cells recognize the host MHC molecules as non-self

109
Q

what is upregulated in immunocompromised hosts?

A

costimulatory molecules because they are susceptible to infections

110
Q

what is specific/adaptive immunodeficiency vs non-specific/innate?

A

specific/adaptive = B and/or T cells are affected
non-specific/innate = innate immunity is affected (Complement, neutrophil defect)

111
Q

what is the origin of primary/congenital immunodeficiency? give an example

A

mutation in genes that allow differentiation of hematopoietic stem cells.
ex: ADA deficiency impairs b and t cell development

112
Q

what is SCID?

A

X-linked Severe combined immunodeficiency: due to mutations in gamma chain of the IL-2 receptor (no T cells, B cells also affected) - thymus problem (primary immunodeficiency)

113
Q

what is X-linked BTK?

A

immunodeficiency disease involved in transducing signals from BCR - bone marrow problem (can’t produce antibodies) (primary immunodeficiency)

114
Q

what is DiGeorge syndrome?

A

thymus does not form, defect in T cell differentiation (primary immunodeficiency)

115
Q

what is hyper-IgM

A

defect in CD40 ligand -> decreases expression of various Igs (primary immunodeficiency)

116
Q

B vs T cell deficiency lead to susceptibility to what respectively?

A

B cells = bacteria
T cells = virus

117
Q

what causes secondary immunodeficiency?

A
  • infectious agents
  • aging and malnutrition
  • malignancy/other diseases/immunosuppressive drugs
118
Q

what are HIV properties? what is the treatment for it?

A

retrovirus transmission through bodily fluids and blood.
anti-retroviral therapy

119
Q

what cells do HIV infect? why?

A

cells with CD4 cell receptors: macrophages, DCs, T cells (main target).
because gp120 on virus recognizes CD4 receptor

120
Q

what co-receptors are needed for HIV to enter cell?

A

CCR5 and CXCR4

121
Q

what does HIV do once it enters the cell?

A

inject RNA genome & reverse transcriptase converts viral RNA genome into pro-viral DNA

122
Q

what makes HIV hard to catch by the immune system?

A

it is highly mutagenic and very error-prone

123
Q

in what cases can HIV stay dormant?

A

if the pro-viral DNA integrates the host genome of an unactivated T cell

124
Q

how does HVC directly kills CD4+ T cells?

A
  1. creates membrane permeability & protein synthesis problems
  2. induces apoptosis
  3. expresses HIV peptides & gets killed by CTLs (cytotoxic T cells)
125
Q

who are naturally immune to HIV infections?

A

people with the rare polymorphism of CCR5 co-receptor which prevents viral infection

126
Q

what are the phases of HIV infection?

A

acute phase = immune system destroys most of the virus
chronic phase = immune response can’t get rid of the infection completely

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