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AIH1 > IMM > Flashcards

IMM Flashcards

1
Q

Innate immunity description

A

Natural, inborn
1st line: physical barriers
2nd line: monophagocyte system, complement, cytokines

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2
Q

How does inflammation start

A

PRR binding –> cellular activation –> phagocytosis –> cytokine release –> inflammation

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3
Q

Acute phase reactant description

A

IL-6 stimulants can be measured (fibrinogen, C3, CRP, haptoglobin)

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4
Q

Neutrophils

A

First to site of injury, phagocytosis, free vs marginate, main cell in pus

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5
Q

Eosinophils

A

Defense against parasites and fungi

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6
Q

NK cells

A

Uses PRR or ADCC (Fc receptors), perforin + granzymes

No memory, short lifespan

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7
Q

Adaptive immunity description

A

Acquired, highly specific, memory, long duration

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8
Q

Th1

A

CD4+
Produces IL-2
Protection against intracellular pathogens
Initiates clonal expansion of CD8+ cells

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9
Q

Th2

A 
CD4+
Produces IL-4, 5, 10, 13
Protection against extracellular pathogens
Regulates B cell class switching
Activated by B cells
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10
Q

Treg

A

Produces IL-10

Maintains tolerance to self antigens

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11
Q

Th17

A

Mediates delayed type hypersensitivity reactions

Inhibits Treg, promotes autoimmune reactions

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12
Q

Cytotoxic T cells

A

CD8+
Perforin + granzymes
Destroys intracellular pathogens + cancer cells

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13
Q

T cell dependent activation

A

2 simultaneous signals, MHC II + CD4+
Most common
B cell isotype switch upon activation

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14
Q

T cell independent activation

A

2 simultaneous signals, PAMP

Inefficient, no memory

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15
Q

Plasma cells

A

No surface Ig
Short lifespan in circulation
Long lifespan in bone marrow

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16
Q

MHC I is located on

A

All nucleated cells

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17
Q

MHC II is located on

A

APCs only

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18
Q

IL-1

A

Pyogenic, initiates acute phase response

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19
Q

IL-2

A

Growth and proliferation of T and B cells

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20
Q

IL-4

A

Promotes Th2 differentiation

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21
Q

IL-5

A

B cell differentiation

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22
Q

IL-6

A

Liver to make APR

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23
Q

IL-8

A

Neutrophil chemotaxis

24
Q

IL-10

A

Calming cytokine released by Treg, suppresses Th2

25
TNFa
Principle mediator of acute phase response
26
SCID
No T or B cells
27
Bare lymphocyte
Defects in MHC expression
28
Wiscott Aldrich
Intrinsic platelet defect
29
DiGeorge syndrome
Thymus not developed
30
B cell deficiencies
Recurrent bacterial infections
31
T cell deficiencies
Severe viral infections
32
Intravascular hemolysis
Decreased haptoglobin Hemoglobinemia, hemoglobinurea Increased LDH Scihistiocytes
33
Extravascular hemolysis
Spherocytes Increased ubil Increased LDH Decreased Hct
34
Mechanisms of complement
Opsonization (90% of the time) | Cell lysis
35
Complement cascade phases
Recognition phase Activation phase: generation of C3 convertase MAC phase
36
Classical pathway recognition phase
Generation of C1qrs complex, activation on C2 and C4 | Calcium dependent
37
Classical pathway activation phase
C4b2a acting on C3 (amplification loop)
38
Lectin pathway
Activated with carbohydrate and MBL
39
Alternative pathway
Continuous hydrolysis of H2O
40
CR1
Transports opsonized immune complexes to fixed tissue macrophages
41
CR2
Binds iC3b, receptor for EBV
42
CR3
Binds iC3b
43
Innocent bystander effect
Once C5678 is formed, C9 binding occurs spontaneously
44
DAF CD55
Inhibits production of C3 convertase
45
C1 esterase inhibitor
Inhibits activation phase
46
Factor H
Dissociates C3bBb from cell surface
47
Factor I
Cofactor with factor H
48
Protectin CD59
Inhibits C9 from binding
49
C1 esterase inhibitor deficiency
Hereditary angioedema, uncontrolled action of C1 on C4 or C2 causing swelling
50
C3 nephritic factor
Continuous complement activation, binds and stabilizes C3bBb, autoantibody found in mesangioglomerulonephritis
51
PNH
Lack of GPI linked proteins (no DAF)
52
Decreased C1q,r,s C4
Large amount of immune complex deposits (SLE, arthritis, Alzheimer)
53
C2 deficiency
Most common in Caucasians, usually not serious
54
C3 deficiency
Repeat infections
55
Properdin deficiency
X linked, increased susceptibility to Neisseria infections
56
Septic shock
Extensive intravascular activation of complement by bacterial endotoxin (increased anaphylatoxins)
57
Deficiency of C' receptors
Similar to C3 deficiency (repeated infections) In affected infants: delayed separation of umbilical cord, recurrent ulcerating infections, abnormal paper thin scar formation

AIH1 (7 decks)

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