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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 ā€“> cellular activation ā€“> phagocytosis ā€“> cytokine release ā€“> 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
Q

TNFa

A

Principle mediator of acute phase response

26
Q

SCID

A

No T or B cells

27
Q

Bare lymphocyte

A

Defects in MHC expression

28
Q

Wiscott Aldrich

A

Intrinsic platelet defect

29
Q

DiGeorge syndrome

A

Thymus not developed

30
Q

B cell deficiencies

A

Recurrent bacterial infections

31
Q

T cell deficiencies

A

Severe viral infections

32
Q

Intravascular hemolysis

A

Decreased haptoglobin
Hemoglobinemia, hemoglobinurea
Increased LDH
Scihistiocytes

33
Q

Extravascular hemolysis

A

Spherocytes
Increased ubil
Increased LDH
Decreased Hct

34
Q

Mechanisms of complement

A

Opsonization (90% of the time)

Cell lysis

35
Q

Complement cascade phases

A

Recognition phase
Activation phase: generation of C3 convertase
MAC phase

36
Q

Classical pathway recognition phase

A

Generation of C1qrs complex, activation on C2 and C4

Calcium dependent

37
Q

Classical pathway activation phase

A

C4b2a acting on C3 (amplification loop)

38
Q

Lectin pathway

A

Activated with carbohydrate and MBL

39
Q

Alternative pathway

A

Continuous hydrolysis of H2O

40
Q

CR1

A

Transports opsonized immune complexes to fixed tissue macrophages

41
Q

CR2

A

Binds iC3b, receptor for EBV

42
Q

CR3

A

Binds iC3b

43
Q

Innocent bystander effect

A

Once C5678 is formed, C9 binding occurs spontaneously

44
Q

DAF CD55

A

Inhibits production of C3 convertase

45
Q

C1 esterase inhibitor

A

Inhibits activation phase

46
Q

Factor H

A

Dissociates C3bBb from cell surface

47
Q

Factor I

A

Cofactor with factor H

48
Q

Protectin CD59

A

Inhibits C9 from binding

49
Q

C1 esterase inhibitor deficiency

A

Hereditary angioedema, uncontrolled action of C1 on C4 or C2 causing swelling

50
Q

C3 nephritic factor

A

Continuous complement activation, binds and stabilizes C3bBb, autoantibody found in mesangioglomerulonephritis

51
Q

PNH

A

Lack of GPI linked proteins (no DAF)

52
Q

Decreased C1q,r,s C4

A

Large amount of immune complex deposits (SLE, arthritis, Alzheimer)

53
Q

C2 deficiency

A

Most common in Caucasians, usually not serious

54
Q

C3 deficiency

A

Repeat infections

55
Q

Properdin deficiency

A

X linked, increased susceptibility to Neisseria infections

56
Q

Septic shock

A

Extensive intravascular activation of complement by bacterial endotoxin (increased anaphylatoxins)

57
Q

Deficiency of Cā€™ receptors

A

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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