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Bpt > Immunology > Flashcards

Immunology Flashcards

1
Q

CD35

A

On RBC, monocytees, granulocytes, B cells

Provides entry for.mycobacteria and leishmania

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2
Q

CD21

A

On B cells

Provides entry for EBV and HIV

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3
Q

CD11b/CD18

A

Provide entry for mycobacteria

On macrophages, NK cell and polymorphs

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4
Q

MAC Inhibitors on cells

A

DAF - delay accelerating factor bracks down C3

HRF - homologous resteiction factor - CD59 prevents formation of MAC on host cells

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5
Q

NK cell killing mechanism

A

Release Perforin or Fas ligand binds to target cells and induces apoptosis
(Fas is also CD95)

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6
Q

NK cell killing mechanism

A

Perforin or Fas ligand induce apoptosis

Fas is also CD95

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7
Q

Alternative name for NK cells

A

Large granular lymphocytes

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8
Q

What cells do NK cells target

A

Virally infected cells
Detect these cells when MHC I is down regulated, inhibiting receptor or activating receptors are on target cell.
Also induce killing by antibody dependent cell cytotoxicity

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9
Q

Positive selection

A

T cells must be able to recognise and bind to self MHC

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10
Q

Negative selection

A

T cells killed in the thymus if the bind too strongly to self MHC to avoid autoimmunity

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11
Q

CRP in innate immunity

A

Binds to c peptide of pneumococcus and triggers complement pathway

acute-phase protein binds to phospholipid in foreign pathogens or damaged host cells

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12
Q

TLR 4

A

Innate receptor that is assocaited with Gram neg septic shock in the setting of release of lipopolysacharride cell wall

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13
Q

TLR 3

A

Deficiency assocuated with HSV encephalitis

-Controls the interferon respnse to dsRNA intermediates of HSV1

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14
Q

IRAK 4 deficiency

A

(Innate)

Recurrent pyogenic infections

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15
Q

Inflammasome Interleukins

A

IL 1

IL 18

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16
Q

FMF gene mutation

A

MEFV (mutation in pyrin gene)

AR , gain of function

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17
Q

NOD 2 in Crohns disease

A

Loss of function

-LEads to more susceptibility to bacteria and less killing of intracellular bacteria leading to granuloma formation

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18
Q

Acute phase response monokines

A

TNF, IL1, IL6

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19
Q

RIG 1 like receptor

A

For detection of cytoplasmic viral RNA

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20
Q

Interferon Type 1

A

Released in response to viral infections
MAin source is plasmacytoid DCs
Interfere with viral replication

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21
Q

TREX 1 gene mutatuon

A

SLE

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22
Q

Lack of antibody response

A

Recurrent sinopulmonary and gut infections
Skin infections
By:
- polysaccharide-encapsulated pyogenic organisms (Strep pneumoniae, H influenza type B, Strep pyogenes, Branhamella catarrhalis)
- Staph aureus
- Giardia lamblia
- Campylobacter jejuni

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23
Q

LAck of T cells

A

Intracellular organism infections

  • Fungi e.g. mucosal Candida, not systemic; pneumocystis (Th17)
  • Viruses e.g. CMV, VZV, HSV; protozoa (CD8)
  • Listeria
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24
Q

Lack of neutrophils/monocytes

A

High grade bacterial infections

  • Staph aureus
  • Gram negative bacteria (E coli, P mirabilis, Serratia marcescens, Pseudomonas aeruginosa and cepacia)

Fungi

  • Invasive aspergillosis
  • Systemic candidiasis
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25
Q

Lack of complement components

A

Classical pathway

  • C1q, C1r, C1s: SLE
  • C4: SLE, GN
  • C2: SLE (50%), vasculitis, GN, recurrent pyogenic infections
  • C3: Recurrent pyogenic infections, CN, immune complex diseases

Alternative pathway
- Properdin, Factor D: Neisseria infections

Terminal components
- C5/6/7/8/9: Disseminated Neisseria infections

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26
Q

Conjugate vaccines attached to a carrier protein and polysaccharide antigen have better efficacy than conjugated vaccine attached to polysaccharide alone. Reason?

A

Addition of the carrier protein to a polysaccharide vaccine makes a polysaccharide vaccine T cell dependent thus boosting the effect of the vaccine

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27
Q

Th1 cell pathway

A

IL 12: naive T cell to Th1
-Induction pathway: STAT4, STAT1, T-bet

Major cytokines

  • IFN gamma
  • IL2
  • IL10
  • TNF Beta

Role in infection:
Intracellular microorganism, AI, proinflammatory, invasive salmonellosis, severe viral infections

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28
Q

Th2 cell pathway

A

IL 4: Naive T cell to Th2

Induction pathway:
-STAT6, GATA3

Major cytokines:
-IL4, IL5, IL9, IL10, IL13, IL25

Role in infection:
-Parasitic, allergic

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29
Q

Th17 cell pathway

A

IL1 and IL6: Naive T cell to Th17

Induction pathway:
STAT3 and ROR

Major cytokines:
-IL17, IL21, IL22

Role in infection:

  • Extracellular bacteria and fungi
  • Autoimmunity
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30
Q

TREG Cell pathway

A

IL2 and TGF Beta: Naive T cell to TREG

Induction pathway:
-STAT 5, Foxp3

Major cytokines
-IL10, TGF Beta, IL 35

Role in infection:
-Tolerance, minimise autoimmunity/allergy/inflammation

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31
Q

Live Vaccines

A 
Yellow fever
MR
Rotavirus
BCG
Japanese encephalitis
Oral Typhoid
VZV
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32
Q

PAracetamol allergy

A
  • Also a weak inhibitor of cyclooxygenase 1 (COX 1)

* Also a weak inhibitor of cyclooxygenase 1 (COX 1)

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33
Q

HLH

haemophagocytic lymphohistiocytosis

A
  • Excessive immune activation
  • Common trigger: EBV
  • macrophages become activated and secrete excessive amounts of cytokines, ultimately causing severe tissue damage that can lead to organ failure
  • NK cells and/or CTLs fail to eliminate activated macrophages.
  • This lack of normal feedback regulation results in excessive macrophage activity and highly elevated levels of interferon gamma and other cytokines.
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34
Q

Which immunoglobulins are inolved in ADCC

A

IgG and IgE

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35
Q

Isotype Definition

A

Variations in the Igs which are present in all members of the family species e.g. IgG1 and IgG2

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36
Q

Immunogen

A

Molecule that elicits an immune response

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37
Q

Hapten

A

Small molecule that alone will not elicit an immune response but will do so when linked to a larger one, called a carrier

38
Q

Epitope

A

Portion of macromolecule to which Ab binds

39
Q

CD20/21

A

Mature B cells (Not plasma cells)

-CD1 also for EBV entry

40
Q

CD19

A

All B Cells (including plasma cells)

41
Q

CD40

A

T and B cell interaction

42
Q

CD3

A

All T cells

43
Q

Best T cells to use for T cell selection

A

Weak binding to MHC (Positive selection)

44
Q

Best T cells for TREG cells for T cell selection

A

Slightly less strong MHC binding

-Not the strongest - those are negative selection

45
Q

Role of AIRE

A

Autoimmune regulator

-Turn on expression of Tissue specific Antigen for T cell selection in thymus

46
Q

APECED

A

Autoimmune Polyendocrine Syndrome 1
(Autoimmune polyendocrinopathy with candidiasis and ectodermal dystrophy)

AR

Due to mutated AIRE gene

47
Q

APECED Triad for presentation

A

Chronic mucocutaneous candidiasis
AI hypoparathyroidism
AI Addisons disease + other AI manifestations

48
Q

2 Signals needed for T cell activation

A
  1. MHC and TCR
  2. CD80/CD86 (B7 molecule) to CD28 for activation
    or CTLA4 for downregulation
49
Q

IPEX

A

Lack of Foxp3 - so no Treg cells
-Global overactivity of immune function (AI, allergy, lymphoproliferative)

DEath as a newborn

50
Q

Superantigen

A

Antigens that stimulate a wide range of T cells - leads to massive cytokine release
-TSS, staph enterotoxins

51
Q

Type 1 Hypersensitivity

A
  • Allergy, immediate
  • Atopy, anaphylaxis, asthma
  • IgE mediated

Fast response (minutes). Free antigens cross link the IgE on mast cells and basophils causing release of Vasoactive biomolectules. Testing can be done with skin test for specific IgE.

52
Q

Type 2 Hypersensitivity

A
  • Cytotoxic, antibody-dependent
  • Autoimmune haemolytic anaemia, rheumatic heart disease, Goodpasture’s, Grave’s, Myasthenia Gravis
  • IgG, IgM, complement, MAC

Antibody inappropriately binds to target host cell (perceived as foreign), leading to cellular destruction via the MAC

53
Q

Type 3 Hypersensitivity

A
  • Immune complex disease
  • Serum sickness, RA, post-strep GN, membranous GN, SLE, hypersensitivity pneumonitis
  • IgG, complement, neutrophils

IgG binds to soluble antigen forming circulating immune-complex that can be deposited in tissues leading to local inflammatory response.

54
Q

Type 4 Hypersensitivity

A
  • Delayed-type hypersensitivity, antibody-independent
  • Contact dermatitis, mantoux test, chronic transplant rejection, MS
  • T-cell mediated

Th1 cells are activated by APCs. When antigen is presented again, the memory Th1 cells activate macrophages and cause inflammatory response.

55
Q

Clinical features of CVID

A 
REcurrent sinopulmonary infections
Chronic or recurrent diarrhea
AI disease
LYMPHOMA, stomach ca
Splenomegaly, granulomatous disease
Allergic disease
Bronchiectasis
56
Q

MX of CVID

A

IVIG monthly

AVOID live vaccines

57
Q

Where does the problem occur in XLA

A

B cell development blockade at Pre B I stage due to BTK mutation

58
Q

Hyperacute rejection

A

AMR pathway

59
Q

Acute rejection

A 
Recipient T cells activated by HLA class 1 donor tissue cells. So CD8 cells attack
-Usually days post transplant
60
Q

Chronic rejection

A

REcipient dendritic cells and monocytes infiltrate the graft

61
Q

What is GVHD

A

Donor T cells attack the patients organs and tissues

62
Q

Clinical features of cryoglobulinemia

A 
Skin purpura
Cutaneous necrotising ulcers
GN
Peripheral neuropathy
Non erosive arthritis
Acral ischemia
Raynaud's
63
Q

Systemic MAstocytosis

A

Proliferative disorder of haematopoetic mast cell progenitors leads to more mast cells on organs

-Due to KIT mutation (D816V mutation)

Higher risk of more severe reactions in venom allergy

64
Q

PEnicillin cross reactivity

A

Amoxycillin, cephalexin, and cefaclor all have the same R1 side chain

65
Q

Hyper IgM Syndrome

A

X linked, CD40L deficiency
Failure of B cell isotype switching and memory B cell generation

Tx:
-IVIG, Bactrim prophylaxis (High risk of PJP), G-CSF

66
Q

Combined immunodeficiency

A

Not as severe as SCID
Ab and T cell deficiency
Worse prognosis than CVID
Mx with IVIG, avoid vaccines

67
Q

Chronic mucocutaneous candidiasis

A

OFten lack of Th17
Onset in childhood
Can be thymoma associated

68
Q

Chronic Granulomatous disease

A

Deficiency in NADPH oxidasse (gp91 on X chromosome)

Clinical:
-Recurrent infections

Tx: Chronic antiboitics, immunisation

69
Q

Activators of alternative pathway

A

Surface bacteria, viruses
Polysacharrides
IgA immune complexes
C3 nephritic factor

70
Q

Activators of Classical pathway

A

IgM, IgG
CRP
C1q

71
Q

Activators of Lectin pathway

A

MBL

Ficolins 1-3

72
Q

Function of complement

A

Cytolysis
Opsonisation (enhance uptake by phagocytes)
Activation of inflammatory response
Immune complex clearing

73
Q

Anaphylatoxins

A

C3a, C4a, C5a

74
Q

List the complements in the different pathways

A

Classical: C1, C2, C4, C3
Alternative: C3, B, D, Properdin (Factor P)

75
Q

SERPING1 gene

A

Need homozygous genes for normal C1 inhibitor amount

76
Q

Hereditary Angioedema

A

Type 1: Reduced C1 inh level

Type 2: Dysfunctional C1 inh - normal level or increased

77
Q

Acquired angioedema

A

Type 1: Associated with B cell lymphoproliferative disorders; Consumption of C1 Inh
Type 2: AI disoders or idiopathic; Ab against C1 inh

C1q levels reduced in acquired not in HAE

78
Q

Tx of HAE:

A

Acute:

  • Purified C1 Inh protein, FFP
  • Icatibant - Bradykinin 2 receptor antagonist
  • Ecallantine: Kallikrein inhibitor

Prevention:
-Anabolic sterodis
Tranexamic acid
C1 INH

79
Q

Protein mutation that is assoicated with atopic dermatitis

A

Filaggrin

80
Q

Why do ACE inhibitors cause angioedema

A

• Angiotensin converting enzyme has at least two physiologic functions.
1. It catalyses the conversion of angiotensin I to angiotensin II (a vasoconstrictor that increases blood pressure)
2. It degrades bradykinin (a potent vasodilator) to inactive metabolites
ACE inhibitors have the effects of DECREASING angiotensin II and INCREASING bradykinin.

81
Q

Causes of Acquired C1 inhibitor deficiency

A

B cell lymphoproliferative disorders
MGUS
Malignancies
AI disorders

82
Q

CD25 + CD4

A

Treg cells

83
Q

IgA deficiency complications

A

Blood transfusions need to be screened

NO LIVE VACCINES

84
Q

Imiquimod TLR

A

TLR 7 agonist

Used in BCC

85
Q

CD16, CD56, CD8

A

NK cells

86
Q

c ANCA

A

PR3

GPA

87
Q

p ANCA

A

MPO

EGPA, microscopic polyangitis, UC, SLE

88
Q

Vaccines recommended in aplenia

A

pneumococcus, meningococcus, haemophilus influzae b and yearly influenza recommended

89
Q

ABx prophylaxis in aplenia

A

§ Amoxicillin daily (250mg) or phenoxymethyl penicillin 250mg BD
§ If allergic take 150mg roxythromycin daily
§ Immuno-competent person – take for 3 years or lifelong
Immuno-compromised- continue lifelong

90
Q

Live Vaccines mneumonic

A

MMR BOYZ Japanese Diarrhea

  • MMR
  • BCG
  • Oral Polio
  • Yellow fever
  • Zoster
  • Japanese encephalitis
  • Oral Typhoid/Rotavirus

Bpt (15 decks)

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