Chapter 6 part 1 Flashcards

1
Q

Factors of Innate Immunity (5)

A
  1. Epithelial barriers
  2. Phagocytes
  3. Dendritic Cells
  4. Complement
  5. NK Cells
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2
Q

Adaptive Immunity (2)

A
  1. B-Lymphocytes => Antibodies

2. T-cells => Effector T-cells

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3
Q

Epithelial barriers (3)

A
  1. Produce antibicrobes - Defensins
  2. Lymphocytes found here
  3. Mechanical stuff
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4
Q

Phagocytes (2)

A
  1. Monocytes/Neutrophils in blood

2. Sense microbe presence and murder invaders

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5
Q

Dendritic Cells (3)

A
  1. Found in epithelium and lymphoid organs
  2. Capture Ags and present to T-cells
  3. Stim cytokine secretion (inflammation and Antiviral response)
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6
Q

Natural Killer cells (1)

A
  1. Early protection (viruses and INTRACELLULAR bacteria)
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7
Q

Mast Cells (1)

A
  1. Release inflammation mediators
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8
Q

Plasma Proteins types (3)

A
  1. Complement system
  2. Mannose binding lectin and C-Reactive protein
  3. Lung Surfactant
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9
Q
  1. Complement system
A
  1. Proteins activated by microbes
  2. Alternative and lectin pathways
  3. classic pathway activated via Abs (adaptive immunity)
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10
Q

Coat microbes and promote phagocytosis?

A

Mannose binding lectin and C-reactive protein

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11
Q

Protection against inhaled microbes?

A

Lung surfactant

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12
Q

How does Innate Rec Microbes?

A

Pattern Recognition patterns (infecting and cell damage activities)

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13
Q

Main Receptors? (2)

A
  1. TLRs

2. NOD-Like receptors (NLRs)

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14
Q

TLRs activate?

A
  1. NF-kB

2. Interferon Regulatory Factors (IRFs)

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15
Q

What does NF-kB do?

A
  1. Stimulates cytokine secretion and expression of adhesion molecules
  2. Results in the attraction of Leukocytes
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16
Q

Interferon Regulatory Factors (IRF

A

Increase Antiviral Cytokine secretion (type 1 interferons)

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17
Q

NLRs are found where?

A

in the cytosol

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18
Q

TLRs are found where?

A

Plasma membranes

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19
Q

How do NLRs signal?

A

Via the inlfammasome

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20
Q

What does the inlfammasome do?

A
  1. Activates Caspase 1
  2. Caspase 1 activates IL-1
  3. IL-1 induces fever
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21
Q

Gain of function mutation in NLR causes what?

A

Autoinflammatory syndrome

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22
Q

How do you treat Autoinflammatory syndrome?

A

IL-1 antagonist duh

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23
Q

NLR may also play a role in (3)

A
  1. Gout
  2. Type 2 Diabetes
  3. Atherosclerosis
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24
Q

Other Receptors? (4)

A
  1. C-Type Lectin
  2. RIG-like R
  3. G-protein coupled R
  4. Mannose R
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25
Q

This receptor is in the cytosol an activate cytokines when stimulated by the NA of viruses?

A

RIG-like R

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26
Q

C-type Lectin are found where?

A

Macrophages and dendritic cells

-In the plasma membrane

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27
Q

Receptor for Neutrophils, Macrophages and Leukocytes?

A

G Protein-Coupled R

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28
Q

Microbial sugars received by?

A

Mannose R

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29
Q

How Does Innate Respond? (3)

A
  1. Inflammation: Cytokines/complement
  2. Antiviral: Type 1 interferons
  3. Stim Adaptive Immunity
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30
Q

Adaptive immunity traits: 2 types

A
  1. Humoral Immunity

2. Cell Mediated Immunity

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31
Q

Extracellular and B-lymphocytes are examples of what type of immunity?

A

Humoral Immunity

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32
Q

T-cells and Intracellular microbes are involved in what type of immunity?

A

Cell-mediated Immunity

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33
Q

What allows Lymphocytes to respond to a wide array of AGs?

A

They have a highly diverse pool of receptors.

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34
Q

B and T cells: general facts (3)

A
  1. Circulate in blood
  2. Considered Naive prior to encountering Ag they are specific for
  3. Once activated they differentiate into Effector and Memory cells
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35
Q

These cells Neutralize Microbes, phagocytose and activate the complement system.

A

B-Cells!

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36
Q

These cells kill infected cells (2)

A
  1. Cytotoxic T Lymphocytes

2. Natural Killer Cells

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37
Q

Regulatory T-cells…

A

…suppress the immune system

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38
Q

Helper T-lymphocytes are activated by?

A

APC-Macrophages (they also activate macrophages themselves) and Dendritic cells

-remember multiples of 8. CD8 = class 1 and CD4 = Class 2 MHC

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39
Q

Helper T-lymphocyte functions?

A
  1. Activate Macrophages
  2. Inflammation
  3. Activate/proliferate T + B lymphocytes
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40
Q

Lymphocyte diversity

A
  1. 1 trillion in healthy adult

2. Not many for each Ag

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41
Q

What is clonal selection?

A

Once a lymphocyte is exposed to a specific Ag, it makes clones that are specific for that Ag.

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42
Q

How is diversity generated?

A

Somatic recombination of genes that encode R. Proteins

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43
Q

When and where does this somatic recombination occur?

A

Durring maturation

T-cells = thymus

B-Cells = Bone marrow

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44
Q

These genes mediate somatic recombination

A

RAG-1 and RAG-2

-Problems result in an inability to generate mature lymphocytes

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45
Q

Recombined T and B cells result in different…

A

TCRs and Igs

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46
Q

If lymphocyte proliferation is polyclonal…

A

…it is considered BENIGN and NON-NEOPLASTIC

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47
Q

If lymphocyte proliferation is neoplastic…

A

it is considered MONOCLONAL and Malignant

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48
Q

3 types of T-lymphocytes

A
  1. Helper T-lymphocytes
  2. Cytotoxic T-cells
  3. Regulatory T-cells
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49
Q

These cells stim activation of leukocytes

A

Helper T-cells

-stim B-cells and thus Ab formation/leukocytes

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50
Q

95% of TCRs are…

A
  1. Heterodimers w/alpha + Beta polypeptide chains

- A/B Rec Ags presented by MHC assure T-cells only see associated Ags

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51
Q

These T-cells don’t need MHCs for activation and where do they aggregate?

A
  1. Gamma-Delta TCR

2. Epithelial surfaces

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52
Q

These cells have TCR receptors for glycolipids presented by MHC-CD1 (MHC-like but not actually) cells

A

NK-t cells can express this TCR

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53
Q

More CD8 or CD4?

A

60% CD4 and 30% CD8

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54
Q

Assist macrophages and B-lymphocytes by secreting cytokines

A

CD4

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55
Q

CD8 cells are?

A

Cytotoxic T-lymphocytes => destroy host cells

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56
Q

MHC 1 bind __

MHC 2 bind ___

A

CD8

CD4

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57
Q

Where do you find B-lymphocytes? (3)

A
  1. Lymph nodes
  2. spleen
  3. mucosa associated lymphoid tissue
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58
Q

B-cell Ag receptor complex consists of?

A
  1. IgM and IgD (membrane bound)
  2. Found on surface of mature Naive cells
  3. After stim by Ag => plasma cells
  4. Igalpha/beta also involved
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59
Q

CR2 and CD21 are examples of?

A

Type 2 complement receptors

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60
Q

What disease uses Type 2 complement receptors to cause its effects?

A

Epstein-barr virus (EBV)

-Infects and enters B-cells through this mech

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61
Q

What receives Th signals?

A

CD40

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62
Q

Dendritic cells “coolest looking according to Dr. G”: Functions/facts

A
  1. APC for T-Cells
  2. Express TLRs and lectins
  3. Recruited by microbes to T-Cell zones
  4. Express high levels of MHC
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63
Q

Dendritic cells in the epithelium/skin are called?

A

Langerhans

64
Q

Where do you find follicular dendritic cells?

A

In germ centers of lymph follikces

-Spleen and lymph nodes

65
Q

What do follicular dendritic cells do?

A
  1. Trap Ags bound to Abs

2. Present Ags to B-cells.

66
Q

Phagocytosis by macrophages is opsonized by? (2)

A
  1. IgG

2. C3b

67
Q

How do T-cells activate Macrophages?

A

IFN-gamma

68
Q

These cells need no previous exposure to destroy tumor and virus cells

A

Natural killer cells

69
Q

NKCs are 5-10% of Lymphocytes and express what on their PM? (2)

A
  1. CD16

2. CD56

70
Q

CD16 is a receptor for what and what does it cause?

A
  1. FC R for IgG

2. Lyse IgG coated cells

71
Q

CD56 is used to do what?

A

Just ID NKCs

72
Q

What TCRs and Igs do NKCs express?

A

None

73
Q

What do NKCs secrete and what does this activate?

A
  1. IFN-gamma

2. Macrophages

74
Q

How is NKC proliferation stimulated?

A
  1. IL-2

2. IL-15

75
Q

What does IL-12 do?

A

activates NKC killing and IFN-gamma secretion

76
Q

What do healthy cells express that stops NK cells from attacking them?

A

Class 1 MHCs

-Unhealthy cells will have reduced class 1 MHC and be attacked

77
Q

How else are NKcells activated?

A

Viruses present activating ligands to NK cells

78
Q

Innate Lymphoid cells (ILCs) are?

A

lymphocytes that lack TCRs but produce similar cytokines

79
Q

What is an example of an ILc?

A

NK cells homes!

80
Q

What do ILCs produce? (5)

A
  1. IFN-gamma
  2. IL-5
  3. IL-17
  4. IL-17
  5. IL-22
81
Q

ILC functions? (3)

A
  1. Early defense against infection
  2. Rec + eliminate stressed cells
  3. Provide cytokines => influence T-cell differentiation
82
Q

These molecules are involved in transplant rejection.

What is another name for them and what chromosome do you find them on?

A
  1. MHC
  2. Human Leukocyte antigens (HLA)
  3. Chromosome 6 (polymorphic = variable)
83
Q

What HLAs are found in MHC class 1?

A

A, B, C

84
Q

Where do you find MHC class 1?

A

All HEALTHY nucleated cells/platelets

-also display cytoplasmic peptides

85
Q

What HLAs associated with MHC class 2?

A
  1. HLA-D (DP, DQ, DR)
86
Q

Where do you find Class 2 MHC and what do they look for?

A
  1. Macrophages, B-cells and Dendrites

2. Internalize Extracellular microbes and soluble proteins into vesicles

87
Q

Key Role of MHC?

A

Regulate T-cell immunity

88
Q

Which cells of innate immunity release cytokines? (3)

A
  1. Macrophages
  2. Dendrites
  3. NK cells
89
Q

Cytokines of innate immunity stimulate? (2)

A
  1. Inflammation

2. Viral attack

90
Q

Cytokines released by innate immunity? (6)

A
  1. TNF
  2. IL-1 (fever)
  3. IL-12 (by NK cells)
  4. Type-1 IFNs
  5. INF-gamma (activate macrophages)
  6. Chemokines
91
Q

Adaptive immunity cells that secrete cytokines?

A
  1. CD4+ T-cells
92
Q

What does CD4 secrete? (5)

A
  1. IL-2
  2. IL-4
  3. IL-5
  4. IL-17
  5. IFN-gamma
93
Q

What do these CD4 cytokines do?

A
  1. Lymphocyte proliferation

2. Differentiation into effector cells

94
Q

These factors stimulate hematopoieses?

A

Colony stimulating factors (CSF)

95
Q

What do CSF produce?

A
  1. GM-CSF

2. IL-7

96
Q

TNF antagonists are given for what disease?

A

Rheumatoid arthritis

97
Q

When would you give cytokines?

A

When you want to stimulate hematopoieses and viral protection

98
Q

Where do Ag samples from lymph go?

A

Lymph nodes

99
Q

Where do Ag samples from blood go?

A

Spleen

100
Q

The lymphocytes in mucosa are mostly…

A

memory cells

101
Q

ABCD acronym for hypersensitivity

A

Type 1: Allergies, Anaphalaxis, Atopy

Type 2: antiBody

Type 3: immune Complex

Type 4: Delayed

102
Q

Hypersensitivity reactions require? (2)

A
  1. Previous exposure (sensitized

2. Imbalance btw effector mech and control

103
Q

Type 1 is?

A

Immediate hypersensitivity

104
Q

What stims type 1?

A

Allergens

105
Q

What happens? (2)

A
  1. Rapid response

2. Ag bind to IgE on mast cells

106
Q

What takes place in the immediate reaction/what is the time frame?

A
  1. min to Hrs
  2. Vasodilation and Vascular leakage
  3. Increased glandular secretions and SM spasms
107
Q

When is the late phase, when does it happen and what are the major cell types? (4)

A
  1. Onset is 2-24 Hrs
  2. Eosinophils = major cells
    (also, neutrophils, basophils, monocytes and CD4+ cells)
  3. Lasts for days
  4. Asthma = example
108
Q

These cells are found near blood vessels, have PM bound granules and crosslinking of IgE = activation

A

Mast cells

109
Q

What receptors bind IgE

A

FCERi

110
Q

When are Mast cells sensitized?

A

When they are covered by IgE

111
Q

What triggers mast cells? (6)

A
  1. C5a and C3a
  2. Chemokines (IL-8)
  3. Drugs (Codeine and morphin)
  4. Adenosine
  5. Melittin (beeeeee venom!!)
  6. Phys stim
112
Q

Steps after allergen binds

A
  1. CD4+ T cells bind to APC (dendrite) and release IL-4
  2. IL4 stims Th2 and class switches B-cells to produce IgE
  3. IL-5 stim eosinophils
  4. IL-13 stim IgE production and increase mucus secretion
  5. Th2 begets more Th2
113
Q

First mediator released by Mast cells?

A
  1. Histamine
114
Q

Histamine function? (3)

A
  1. SM contraction
  2. Vasc Permeability
  3. Increased Mucus Secretion
115
Q

What types of enzymes are stim by Mast cells?

A
  1. Neutral proteases (chymase and tryptase)
  2. Hydrolases
    - Enzymes cause tissue damage
116
Q

Proteoglycans stimulated by Mast cells?

A
  1. Heparin (anticoagulant)
117
Q

Lipid Mast Cell mediators activate?

A

Phospholipase A2

118
Q

Phospholipase A2 stimulates production of? (3)

A
  1. Leukotrienes C4 and D4
  2. Prostaglandin D2
  3. Platelet activating factor (PAF)
119
Q

These cause bronchospasms and increase mucus production.

A

Prostaglandin D2

120
Q

What is the importance of Leukotrienes C4 and D4?

A
  1. The are the most potent vasoactive and spasmogenic agents (1000x Histamine)
121
Q

PAF does what?

A
  1. Platelet aggregation
  2. Release of histamine
  3. Bronchospasms
  4. Increased vasc perm + vasc dilation
122
Q

Cytokines produced by Mast cell? (4)

A
  1. TNF
  2. IL-1
  3. Chemokines
  4. IL-4
123
Q

What cytokine(s) amplifies TH2 response?

A

IL-4

124
Q

Cytokine(s) involved in late phase leukocyte recruitment and epithelial damage

A

TNF, IL-1 and Chemokines

125
Q

Prominent cell in late phase reactions?

A
  1. Eosinophils
126
Q

How do Eosinophils cause tissue damage?

A
  1. Proteolytic Enzyme
  2. Major Basic Protein
  3. Eosinophil Cationic Protein
127
Q

What do you need for Lat-phase Tx?

A

Broad spectrum anti-inflammatory

Antihistamine is more acute

128
Q

What is Atopy?

A
  1. Increased propensity for immediate hypersensitivity reaction
  2. Increased serum IgE and IL-4
  3. Chrome 5 + 6 linked to genetic propensity
129
Q

Non-atopic allergies?

A
  1. temp/exercise
  2. No TH2 or IgE
  3. Mast cells are increasignly sensitive
130
Q

Systemic anaphylaxis is “important to know about”

What does it result in?

A
  1. Vask shock w/in min
  2. Widespread Edema and itching rash
  3. Difficulty breathing with contracting airways
131
Q

What is Type II?

A
  1. Ab-Mediated Hypersensitivity

2. AutoAbs specific for norm tissue

132
Q

How do Ab mediate injury?

A
  1. Opsonization (C3b) + phagocytosis
  2. Complement (C3a + C5a) and Fc receptor Mediated inflammation
  3. Ab-mediated cell dysfunction (anti-receptor Abs disrupt function)
133
Q

Specific Ab-mediated cell dysfunction for Myasthenia gravis

A
  1. AcH-R Abs => M. weakness + paralysis block N-M transmission
134
Q

Ab-mediated dysfunction for Graves disease

A

TSH-R Abs => Hyperthyroidism

135
Q

Autoimmune hemolytic anemia causes?

A

Opsonization of RBC and eventually anemia

136
Q

Hemolytic disease of newborn

A

Erythroblastosis Fetalis

137
Q

What causes Erythroblastosis Fetalis?

A

Maternal IgG, anti-erythrocyte Abs cross placenta and destroy RBC

138
Q

Diseases with Abs to own blood cells? (3)

A
  1. Hemolytic anemia
  2. Agranulocytosis
  3. Thrombocytopenia
139
Q

Ab can also cause tissue damage in what kidney disease?

A

Glomerulonephritis

140
Q

Ab reactions/type 2 are also common in what type of reactions?

A

Transfusions

141
Q

Type 3 is involved with…?

A

The Immune Complex

142
Q

What is the immune complex?

A

Ag-Ab complex that causes tissue damage and inflammation

143
Q

3 things associated with hypertension and the immune complex?

A
  1. Kidney (glomerulonephritis)
  2. Joints (arthritis)
  3. Small blood vessels (vasculitis)
144
Q

1 more disease associated with Type 3

A

Lupus

145
Q

What is the pathogenesis of the Immune complex?

A
  1. Complement fixing IgG and IgM
  2. Complement proteins at injury site
  3. Consumption of complement (reduce C3 levels)
146
Q

What does IgG and IgM fixing do?

A

produces lesions

147
Q

What are type 4 reactions?

A

Delayed/T-cell mediated

148
Q

Inflammation is produced by…

A

CD4 and CD8

149
Q

Diseases associated w/type 4 (5)

A
  1. Rheumatoid arthritis
  2. MS
  3. Type 1 diabetes
  4. Inflammatory bowl disease
  5. Psoriasis (scaly rash)
150
Q

Stim Th-1 leads to production of?

A

IFN-gamma

151
Q

Stim Th-17 leads to production of?

A

IL-17, IL-22 and chemokines

152
Q

How does IFN-gamma stim macrophages?

A
  1. Increase ability to phagocytose
  2. Increase MHC class 2 expression
  3. Secrete TNF, IL-1 and chemokines (inflammation)
  4. Produce more IL-12 (stim TH-1 production)
153
Q

Example of delayed th reaction?

A

Tuberculin Reaction (prev sensitized = reddening after 8-12 hrs)

154
Q

TB infection quick facts (4)

A
  1. Non-degradable Ags
  2. Colonizes lungs
  3. Infiltrate dominated by macrophages
  4. Macrophages cause granulomas if sustained!!!
155
Q

Cytokines characteristic of Granulomatous inflammation (2)

A
  1. Increased TH1

Increased IFN-gamma

156
Q

What can be CD8 mediated? (2)

A
  1. Type 1 diabetes

2. Graft Rejections

157
Q

Define Dysbiosis

A

Alteration in microbiom (less good and more bad)