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FRACP Shuyu > Immunology > Flashcards

Immunology Flashcards

1
Q

Most common class of primary immunodeficiency

A

Antibody disorders

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2
Q

What type of PID does bacterial infections suggest

A

antibody deficien

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3
Q

What types PID gets infections with encapsulated organisms

A

complement and splenic function

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4
Q

Initial investigations in primary immunodeficiency

A

full blood count
immunoglobulins
serum protein electrophoresis
HIV

addition:
complement (C3,4, CH 100 and AH50)
lymphocyte subsets
urinalysis

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5
Q

Primary immunodeficiency disorders with absent B cells

A

X-linked agammalobulinaemia and 5-10% of CVID

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6
Q

How to test for functional antibodies

A

Response to polysaccharide or conjugated vaccination

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7
Q

Clues to phagocyte defect

A

lung, bones, soft tissue

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8
Q

Wiskott-Aldrich syndrome

A

Eczema, thrombocytopenia, immunodysfunction

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9
Q

Ataxia-telangiectasia

A

Defect in the ATM gene (impaired DNA repair)

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10
Q

DiGeorge anomaly

A

Chromosome 22q11

Thymic defect with cardiac, cleft palet, hypoparathyroidism

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11
Q

Hyper-IgE syndrome (HIES or Job syndrome)

A

Eczema, skin abscesses, lung infections, eosinophilia and high serum IgE

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12
Q

Primary lymphoid tissue (2)

A

bone marrow and thymus

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13
Q

Secondary lymphoid tissue

A

Spleen, lymph nodes, mucosal lymphoid tissue

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14
Q

What T cells does MHC II and MHC I turn on

A

MHC II CD4

MHC I CD8

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15
Q

Positive selection in T cell production

A

Selective T cell receptors that weakly recognises the self MHC receptors

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16
Q

What stimulates TH1

A

IL-12

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17
Q

What does TH1 make and what does it do

A

Makes interferon gamma

Turns on macrophages, NKC, B cells, immunoglobulin production
The macrophages make IL-1, IL-6, TNF

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18
Q

Purpose of TH2

A

Targets helminth/parasites

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19
Q

What Thelper is associated with allergy

A

TH2 (through the production of mast cells)

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20
Q

PAMPs and DAMPs

A

Patterns that stimulate innate arm of the immune response

Pathogen-associated molecular patterns

  • Structures that are never found outside of bacteria/virus/fungus
  • E.g. toxins, flagellin, peptidoglycans, LPS, RNA and DNA

Danger associated molecular patterns

There is also HAMPs

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21
Q

Pattern recognition receptors

A

Part of the innate immune system

Can be membrane bound or soluble

Targets structures that are only expressed on micro-organisms
E.g. C1q, CRP, Mannose binding lectin, TLR4

Triggered by pathogen associated molecular patterns (PAMPs) and danger/damage associated molecular patterns (DAMPs)

Soluble PRRs include antimicrobial peptides
They are also complement activators
- Classical pathway: CRP< C1q
- Lectin pathway: Mannose-bind lectin, Ficolins
- Alternate pathway: Foreign surface (lacking complement control proteins)

Lead to signalling/response or blockade/complement activation

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22
Q

What is cathelicidin LL-37 and what disease pathologies is it involved in

A

Cathelicidines (LL-37 is the only member in humans) is an antimicrobial peptide (AMPs) produced by circulating cells and epithelial surfaces as a part of the innate immune system.

Cathelicidin LL-37 is overexpressed in psoriasis and underexpressed in atopic dermatitis
Th17 deficiency in CMC (chronic mucocutaneous candidiasis)- failure to secrete defensins-> candida susceptibility

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23
Q

CRP function

A

innate immune system because it binds to pneumococcus

it arises in acute phase response

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24
Q

mannose-binding lectin (mbl) deficiency

A

Acute phase protein
Binds widely to iligosaccharids
Complement activation via lectin pathway - cleaves C4 and C2
Opsonin - facilitates uptake by macrophages

MBL deficiency

  • quite common (low levels in 8%)
  • not severe
  • increase susceptibility/severity to a range of diseases
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25
Q

How does lipopolysacchariedes (LPS) signalling cause septic shock

A

LPS (released by gram negatives) binds CD 14 which binds to toll-like receptor 4, and signals an acute inflammatory mediated event (via TNF, IL6 and other cytokines) where the monocytes churns out more cytokines and causing septic shock

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26
Q

Toll-like receptors function

A

can be intracellular and extracellular
stimulated by IL-1
act via NF-kappaB which acts on promoter regions on antimicrobial peptides
Also release cytokines/chemokines and expression of co-stimulatory molecules

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27
Q

Gram negative sepsis shock pathophysiology

A

toll-like receptors

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28
Q

C-type lectins and its role in HIV

A

A type of PRR. Recognises carbohydrates on pathogens and causes phagocytosis

The dendritic cell captures HIV via DC-SIGN
The dendritic cell goes to the lymph nodes ??? don’t quite understand

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29
Q

Dectin-1 and dectin 2

A

major receptors for fungae

directs APC to TH17

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30
Q

Intracellular PRRs

A

TLR
NLD - NOD like receptors
RLR
ALR

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31
Q

NOD-like receptors roles (4)

A

4 major roles:

  • Inflammasome assembly (sense pathogens and danger and fire off caspas-1 that release IL-1 and IL18).
  • Signalling NF-kappaB and MAPK (part of the RAS/MEK) pathway
  • Induction of MHC-I/II expression
  • Autophagy - capture and digest intracellular bacteria
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32
Q

Role of inflammasome in gout

A

The crystals in gout get phagocytosed. They are recognised by inflammasomes. That turns on caspase-1 and then IL-1 causing acute inflammation

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33
Q

Inflammasomes in Familial Mediterranean Fever

A

FMF is an autosomal recessive condition that has a gain-of-function mutation in the pyrin gene.

Pyrin is normally inactivated by cytosol homeostasis. However, when the Pyrin inflammasome gets activated (normally does so when there are Bacterial products in the cytosol), it generates IL-1 and IL-18.

Clinical presentation:
Recurrent episodes of fever, raised CRP, inflammation, serositis, arthritis, amyloidosis

It is treated with colchicine, which inhibits microtubule formation and uncouples inflammasome activation.

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34
Q

Crohn’s disease and NOD2

A

NOD2 is expressed in Paneth cells (in the terminal ileum). It is activated by muramyl dipeptide (MDP) from gut bacteria. NOD2 signals via NFkB and stimulates release of AMPs and autophagy.

A proportion of Crohn’s has mutations in NOD-like receptors (homozygotes have 17.1 increased risk of Crohn’s), resulting in a failure of the intestines to protect itself from microbiota. The failure of autophagy leads to decreased killing of intracellular bacteria and causes formation of granulomas.

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35
Q

Acute phase response induced by 3 monokines

A

TNF
IL-1
IL-6

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36
Q

What do the 3 acute phase response monokines target

A

TNF
IL-1
IL-6

Acts on the liver

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37
Q

IL-1

A

Fever

Stimulates IL-1

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38
Q

What blocks IL-1

A

anakinra

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39
Q

IL-2

A

T-cell expansion

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40
Q

what cytokine has a role in inducing a generalised anti-viral state of cellular metabolism i other cells

A

Type 1 interferons

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41
Q

What releases Type 1 interferons

A

Plasmocytoid dendritic cells

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42
Q

What detects DNA in cytoplasm

A

AIM2 inflammasome

cGAS

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43
Q

What simulates inflammasomes

A

NOD like receptors

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44
Q

What does macrophages differentiate from

A

monocytes

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45
Q

What cells generate oxygen radicals

A

macrophages and neutrophils

- they also fuse with lysosomes with antimicrobial enzymes and proteins

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46
Q

what does NADPH oxidase do

A

generate oxygen radicals to kill microbials

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47
Q

NETosis

A

neutrophils die by NETosis and extrude DNA webs that trap bugs

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48
Q

ILC - innate lymphoid cells

A

Derived from lymphoid progenitor
Populate various tissue sites where they police activity
They respond to signals sent by epithelium under stress by producing cytokines
They produce the same cytokines as T-helper cells
The cytokines determine how T-helper cells differentiate

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49
Q

ILC-2 pathology

A

role in asthma, allergic rhinitis, eosinophilic oesophagitis, atopic dermatitis

allergens process alarment IL-33, turning on ILC-2 which produces IL-4 and turns on Th2

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50
Q

What are NK cells a subset of

A

ILC-2

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51
Q

What do NK cells do

A

Kill cell infected by virus and tumour cells

They detect virus infected cells by detecting that the MHC I has been turned off or antibody bound to target cells

They release a lot of inflammatory cytokines (INFapha, IL12, 15, 18)
Release INFgamma which stimulates macrophages and TH1 cells

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52
Q

Difference between NKs and T cytotoxic cells causing cytotoxicity

A

NK cells respond to a lack of MHCI

T cytotoxic cells senses viral particles which are presented to the surface of the infected cell

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53
Q

chemokines

A

cytokines that direct the movement of leukocytes

Released from tissue sites and bind chemokine receptors on leukocytes and govern leukocyte migration

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54
Q

What are the 2 receptors required for HIV to enter a T cell

A

CCR5 and CD4

however it can later mutate to use CXCR4

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55
Q

adhesion cascade

A

the leukocyte is rolling along activated endothelium
CAM (cell adhesion molecules) bind integrins and cell adhesion molecules
the cell then moves through the endothelium into the tissue itself

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56
Q

Leukocyte adhesion deficiency

A

Defect in the integrins or deficiency of selections (cannot roll along endothelium)

Present with bad tissue bacterial infections (but with abundant leukocytes in circulation)

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57
Q

what band on protein electrophoresis represents antibodies

A

gamma band

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58
Q

light chain ratios in humans

A

2 kappa: 1 lambda

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59
Q

How many hypervariable regions are there in an IgG

A

12

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60
Q

IgG subclasses

A

IgG 1-4

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61
Q

What IgG has good blocking function

A

IgG4

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62
Q

What isotype crosses the placenta

A

IgG

protects neonates for the first 6 months of life

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63
Q

function of IGA

A

protection of mucosal surface

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64
Q

what transports IgA

A

plgR

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65
Q

how does immunisation to tetanus work

A

by neutralising the toxin

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66
Q

neonatal immunoglobulins

A

Maternal IgG transported during gestation
Neonates make IgM first then
Neonatal then synthesizes new IgG
Lastly IgA?

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67
Q

Isotypes, allotypes and idiotypes

A

isotypes are different Igs (IgG, IgM etc)
Allotypes - differences in the constant regions
Idiotypes - variations in the antigen-binding region

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68
Q

where do NK cells develop and what does they come from

A

fetal liver

ILC/common lymphoid progenitor cells

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69
Q

which antibody chain has diversity segments

A

Heavy chain but not light chain

They both have V and J

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70
Q

what is a marker in newborn for B-cell primary immunodeficiency

A

TRECs/KRECs

(quantitivate PCR) for SCID

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71
Q

Pre-B cell receptor

A

heavy chain pairs with 2 surrogate light chain

sends signalling for further maturation

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72
Q

what antibody is the immature B cell

A

Immature B cell is derived from the Pre-B cell

It has IgM

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73
Q

What antibodies are on the mature B cell

A

IgM and IgD (same antigen specificity)

It is naive until it becomes antigen experienced

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74
Q

BAFF and APRIL

A

expressed on antigen presenting cells

BAFF promotes survival for B cells
Upregulates TLR
Promotes immunoglbulin class switching
Memory B celldifferentiation to plasma cells

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75
Q

What autoimmune diseases are associated with elevated levels of serum BAFF

A

autoimmune hepatitis, PBC, SLE

monoclonal antibodies: belimumab, atacicept, blisibimod

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76
Q

what are the mechanism action of belimumab, atacicept, blisibimod

A

inhibitor of BAFF and APRIL to reduce B cell survival and reduce autoreactive B cells in SLE

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77
Q

which locus does antibody class switching occur

A

In the heavy chain locus, not the VDJ region

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78
Q

What B cell does CLL derive from

A

memory B cells

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79
Q

absolute antibody of T cells

A

CD3

80
Q

what does the TCR on Tcytotoxic attach to

A

TCR attaches to MHC I

81
Q

Autoimmune regular (AIRE)

A

turn on tissue-specific antigens are low levels in the thymus and allow deletion of high-affinity T-cells and induction of thymic regularly T ells
leads to negative selection

82
Q

Autoimmune polyendocrine syndrome Type 1

A

Autosomal recessive disorder due to mutatedAIRE gene- failure to delete T-cells specific for multiple tissue antigens
Leads to autoimmunity

3 cardinal features:

  • autoimmune hypoparathyroidism
  • autoimmune addison’s disease
  • chronic mucocutaneous candidiasis (due to cells that produce cytokines that are protective against candidiasis - IL 17/22 antibodies)
83
Q

which cells do somatic hypermutation occur

A

The v region in the immunoglobulin loci for B cells

84
Q

What is the second signal in T cell activation

A

The APC produces B7.1 and B7.2 (CD80 and C86) which binds to CD28

85
Q

What is delayed deactivation/T cell exhaustion

A

CD80 and CD 86 binding with CTLA-4 and turns off activated T cells

86
Q

What drugs targets IL-2

A

Steroids
Calcineurin inhibitors (inhibits IL-2 induction)
stops T cell expansion

87
Q

What interleukin is vital for generation and maintenance of regulatory T cells

A

IL-2

88
Q

Autoimmune lymphoproliferative syndrome

A 
Defect in Fas pathway of T-cell paoptosis
Fas is like a suicide button on a cell
Clinical manifestation:
- lymphoproliferation
- autoimmunity esp immune cytopenias
89
Q

What markers do Treg cells have

A

CD4+
CD25 (interleukin 2 receptor alpha chain)
foxp3 (master regulator of Treg cells)

90
Q

Super antigens

A

Bind outside the MHC to a V-beta and MHC chain and is able to turn on a huge proportion of T cells

e.g. toxic shock syndrome

91
Q

what T helper cells drive neutrophil infiltration

A

Th17

92
Q

Th1 secretes

A

IFN-gamma, TNF

93
Q

Mendelian susceptibility to mycobacterial disease

A

Genetic deficiency to amount Th1 response

94
Q

What Th cells is involved in the atopic pathway

A

Th2 cells
Makes IL 4, 13 which target B cells to make IgE
Makes IL5 which makes eosinophils

95
Q

what Th cell has a pathogenic role in psoriasis

A

Th17

IL17 inhibitors e.g. secukinumab, ixekizumab, brodalumab

96
Q

what corrollates with disease activity in Allergic Bronchopulmonary Aspergillosis

A

IgE

97
Q

What is early phase response drive by in allergen challenge (e.g. asthmatics)

A

Mast cells (steroid resistant)

98
Q

Clinical manifestations from PIDs from lack of antibodies

A

Recurrent sinopulmonary and gut infections

Organisms: standard organisms that cause these problems

99
Q

Lack of T cells clinical manifestations

A

Same as AIDs sx

  • Fungi - mucosal candida (lack of Th17)
  • Viruses
100
Q

Lack of neutrophils clinical manifestations

A 
High-grade bacterial infections
Fungal infections (systemic vs lack of T cells which is more just mucosal involvement)
101
Q

Complement deficiency clinical manifestations

A

If lacking classical pathways, get lupus and other autoimmune diseases

If lacking terminal components - disseminated neisseria infections

102
Q

X-linked agammaglobulinaemia (Bruton’s agammaglobulinaemia)

A

Mutation in Bruton’s TYR kinase (Btk)

Early onset and no B cells and no lymphoid tissue

Most common cause of defect in B cell development

103
Q

What antibody deficiency is coeliac’s disease associated with

A

IgA

  • measure TTG antibody (which is a subset of IgA)
  • That’s why need to also measure IgA
104
Q

How to treat IgA deficiency

A

No IVIG
Prompt ABx
Transfusion with IgA deficient blood

105
Q

Hyper IgM syndrome

A 
Lack of CD40 to CD40L signal (between B and T cell)
Fail to class switch

Onset 1-2 years
Recurrent respiratory infections

106
Q

the activation and cleavage of which of the following early complement components is most likely to elicit an inflammatory response

A

C3

107
Q

Why does complement not bind to self

A

Complement control proteins

108
Q

C1 esterase inhibitor deficiency pathology

A

hereditary angiooedema

hemizygous deficiency

Uncontrolled activation of classical pathway and other pathways
Increased bradykinin release and binds bradykinin B2 receptor

The bradykinin increases capillary permeability and oedema

C4 and C2 go down due to activation and consumption

109
Q

Classification of hereditary angiooedema

A

Type I - mutation prevents production of C1-INH (low levels)

Type II - Dysfunctional protein (normal levels)

Differentiate w functional assay of C1 inhibitor

There are also rare other genes but mainly C1-INH

110
Q

Causes of acquired C1-inhibitor

A

Type I - B cell lymphoproliferative disorders resulting in consumption of C1-inhibitor

Type II - associated with autoimmune disease or idiopathic - autoAb against C1-INH

111
Q

Hereditary angiooedema C3/4 results

A

Reduced C4, normal C3

112
Q

Treatment of hereditary angiooedema

A
  1. Purified C1-INH protein

2. Bradykinin-2 receptor antagonistIcatibant

113
Q

Complement deficiency associated with pyogenic infections

A

C3

114
Q

Deficiency of complement regulatory proteins (CD59, CD55) causing red cells to be attacked by complement system

A

Paroxysmal Nocturnal Haemoglobinuria

115
Q

PNH pathophysiology

A

Mutation in haemotopoietic stem cell - PIG-A
PIG-A normally links proteins to the surface of cells (CD55 and CD 59)
Eventually the cell gets lysed

116
Q

Atypical HUS

A

Triad of

  • Microangiopathic haemolysis
  • Thrombocytopenia
  • Renal failure

Typical HUS caused by action of shiga toxin of E. Coli
Atypical HUS is caused by genetic mutations of alternate pathway

117
Q

Eculizumab

A

Monoclonal antibody against C5 and blocks further attacks of membrane lysis complex

Role in PNH
Atypical HUS

118
Q

which chromosome is the MHC encoded

A

chromosome 6

119
Q

HLA class I molecules

A

HLA-A, B, C

120
Q

What cells do not have HLA I

A

RBC, some neuronal cells

Higher expression on WBC

121
Q

beta2 microglobulin

A

Reflects cell turnover, associated with poor prognosis for MM

Non covalent bond to long chain as a part of HLAI

122
Q

HLA class II

A

DR, DQ, DP

On antigen presenting cells

123
Q

Where does the CD4 bind to on the HLA II

A

Beta-2 domain

124
Q

How many genes encode each of HLA II

A

2 genes per HLA - alpha and beta chains

125
Q

HLA and drug hypersensitivity:

Abacavir

A

HLA B*57:01

126
Q

HLA and drug hypersensitivity:

Carbamazepine

A

HLA-B15:02 and HLA-A31:01

127
Q

HLA and drug hypersensitivity:

Allopurinol

A

HLA-B*58:01

128
Q

What HLA does platelets express

A

HLA class I

129
Q

Transfusion related acute lung injury mechanism

A

HLA antibodies from blood donor react against the patient receiving the transfusion

130
Q

What are the 3 antigen presenting cells

A

Dendritic cells
Macrophages
B cells

131
Q

TAP protein

A

TAP = transporter associated with antigen processing

They mediate peptide transport to eventually present the antigen on MHC I

132
Q

Disease that inhibits TAP protein

A

HSV - stops antigen presenting

133
Q

3 types of dendritic cells

A

Follicular dendritic cell (role in B cell selection)
Classical dendritic cells (capturing antigen and delivering to T cells)
Plasmacytoid dendritic cells (churns out interferon in response to viral infections)

134
Q

Mechanism of immunotherapy for allergy

A

Small amounts of allergen leads to immune deviation to Th1 phenotype rather than Th2

135
Q

Diagnosis of food allergy - role of skin prick

A

Rough correlation between size of wheal and likelihood of allergy

136
Q

How often does childhood milk and egg allergy persist into adulthood

A

20%

137
Q

Anaphylaxis diagnosis

A

Serum tryptase - peaks at 60-90 minutes and persists up to 5 hours

+ clinical:
acute skin/mucosal involvement and at least one of the following
- respiratory compromise
- reduced blood pressure

138
Q

Biggest predictor of poor outcome in anaphylaxis

A

Asthma

139
Q

Diagnosis of venom allergy

A

Skin prick and intradermal testing

but noted not for food

140
Q

Mastocytosis

A

Proliferative disorder of haemopoietic mast cell progenitors

HIgh risk of anaphylaxis and more severe reactions

Mutation in kit, a tyrosine kinase receptor

Baseline high tryptase levels

141
Q

what anaesthetic medication can you not skin test

A

opioids because they are a natural mast cell degranulator

142
Q

mechanism of ACE-I angiooedem

A

ACE normally breaks down bradykinin into an inactive metabolite

In ACE-I, there is defective bradykinin degradation

143
Q

Chronic idiopathic urticaria duration criteria time frame

A

> 6 weeks

144
Q

Treatment for chronic idiopathic urticaria

A

Non-sedating H1 antihistamines (50% refractory)
No benefit in H2 antagonist
Omalizumab 300mg s/c q4weeks
Cyclosporine

145
Q

Omalizumab

A

recombinant monoclonal antibody that forms complexes with free IgE to preventit from binding to mast cells

146
Q

does bactrim and frusemide have cross-reactivity

A

unlikely because those allergic to bactrim are allergic to the specific antibiotic side chain (which is not present on frusemide)

147
Q

Takayasu’s arteritis - what kind of vasculitis and pathophysiology

A

Chronic inflammatory granulomatous aortitis
(Large vessel vasculitis)

Driven by T cells, IL-6

148
Q

What viral infection is polyarteritis nodosa associated with

A

Hep B (also ass w HCV, HIV, hairy cell leukaemia)

149
Q

Polyarteritis nodosa - type of vasculitis and pathophysiology

A

Systemic necrotising vasculitis of medium-sized muscular arteries

ANCA negative

150
Q

Granulomatosis with polyangiitis (GPA) clinical sx

A

ENT, pulmonary, renal

ANCA +

151
Q

Eosinophilic granulomatosis polyangiitis ANCA

A

ANCA only 50%, usually MPO >100

152
Q

vasculitis associated with rapid progressive AKI (acute GN picture)

A

Anti-GBM

153
Q

IgA vasculitis

A

Henoch Schonlein Purpura

154
Q

Cold induced acrocyanosis + necrotic cutaneous ulcers

A

Cryoglobuinaemia

155
Q

What is hyperacute rejection mediated by

A

Anti-A and anti-B antibodies

Anti-HLA antibodies (from previous exposure to foreign HLA proteins)

156
Q

Direct pathway in transplant rejection

A

Acute rejection

Recipient T cells (cytotoxic > helper) is activated by HLA class on donor tissue cells 
Involved 1-10% of T cells (storng response)

Also reacts with HLA class I molecules on donor dendritic cells

157
Q

Indirect pathway in transplant rejection

A

Chronic rejection
Recipient dendritic cells infiltrate the graft and place donor APCs
They present graft antigens on self HLA and activate Th cells which activate an antibody response
<0.1% of total T cell repertoire

5% graft failure/year

158
Q

HLA matching in solid organ transplant vs haematopoietic cell transplants

A

HSCT requires better HLA matching to improve graft survival and reduce GVHD
-/12 match

159
Q

GVHD mechanism + what prophylaxis is used

A

Donor T cells react against recipient tissues/organs

T-cell depletion

160
Q

What does T-cell depletion in HSCT increase the risk of

A

Leukaemic recurrence

161
Q

Mechanism of action of glucocorticoids as an immunosuppressant

A
  1. Binds to glucocorticoid receptor and alters transcription and intercepts 2nd messengers
  2. Inhibit the synthesis and release of:
    - IL-1, TNF, IL-2, INF-gamma
    - Prostaglandins, leukotrienes
    - Plasminogen activator
162
Q

Azathioprine

A

Stops clonal expansion of immune response as the metabolites are incoorporates into ribonucleotides - lymphocytes
Inhibits CTL/NK

Metabolised to 6-mercaptopurine and thioguanine

163
Q

Calcineurin inhibitors

A

When a T cell receptor is activated, signalling cascades are activated and calcium is fluxed from outside to intracellular which binds to calcineurin which rephospharylates NF-ATc which causes IL-2 to be produced.

Cyclosporin binds to cyclophilin and tacrolimus binds to FKBP which both inibits cyclophilin.

They are T cell selective

164
Q

Mycophenolate

A

Affects leukocytes by inhibiting cell division through inhibition of IMPDH which is necessary for generation of guanine nucleotides

165
Q

Methotrexate

A

Inhibits dihydrofolate reductase which decreases tetrahydrofolate and synthesis of thymidylate
Inhibits DNA synthesis

166
Q

Cyclophosphamide

A

Alkylating agent and alters DNA

Affects Lymphocytes B>T and plasmas

167
Q

Sirolimus

A

Inhibits mTOR

Also binds to FKBP (like tac)

168
Q

3 main inflammatory cytokines and their actions

A

TNF - activates endothelium, increases vascular permeability, fever, mobilisation of metabolites, shock
IL-1 - fever, IL-6 production, increase expression of adhesion molecules
IL-6 - fever, haematopoiesis, activates osteoclasts, lymphocyte activation

169
Q

Anti-TNF examples

A

Infliximab, adalimumab, golimumab

Etanercept

Certolizumab pegol

170
Q

IL-1 examples

A

Anakinra
Canakiinumab
Rilonacept

171
Q

IL-6 examples

A

Tocilizumab

Siltuximab

172
Q

Abatacept

A

CTLA4-Ig = B7 blocker

Prevents T-cell activation

173
Q

Difference between ipilimumab and abatacept

A

They both try to stimulate T-cells

Abatacept is a CTLA4-ig which blocks B7 and prevents activation

Ipilimumab is a CTLA4 blocker which stops T-cells from being inactivated

174
Q

Integrin blockers

A

Vedolizumab

Natalizumab

175
Q

What are mannose-binding lectin (MBL) and ficolin involved in

A

Lectin in the complement pathway

176
Q

Chronic mucocutaneous candidiasis

A

Th17 deficiency –> failure to secrete defensins (a type of antimicrobial peptides - AMPs) –> candida susceptibility

177
Q

How are toll-like receptors implicated in autoimmunity

A

TLR signalling in B cells can promote autoantibody formation

May explain targeting of nucleic acid (ANA, dsDNA) in lupus

178
Q

How does HIV from the mucosal surface get transported to infect T cells

A

Dendritic cells express a C-type lectin called DC-sign
It captures HIV-1 at sites of mucosal entry
The DC then migrates to the lymphoid tissues and transmits HIV-1 to T Cells

179
Q

What do inflammasomes do?

A

They sense PAMPs and DAMPs and activate caspase-1 and releases IL-1 (and less importantly IL-18)

180
Q

What is released by the liver to prevent tissue destruction in the acute phase response

A

Alpha1-anti-trypsin

181
Q

What do interferon type 1s do

A

Interferon alpha and interferon beta

Pasmacytoid dendritic cells are a particularly potent source
They interfere with viral replication by acting in the interferon receptors:
- Induce resistance to viral replication in all cells
- Increase MHC-I expression and antigen presentation in all cells
- Activate DC and macrophages
- Activate NK cells

182
Q

RIG-I-like receptors (RLRs)

A

A type of pattern recognition receptors: detects viral RNA in the cytoplasm

183
Q

AIM2/cGAS

A

Types of pattern recognition receptors that detected viral DNA in the cytoplasm

184
Q

Which innate immune system cells are phagocytes

A

Macrophages (derived from monocytes)

Neutrophils

185
Q

What pattern of infections do B-cell defects pre-dispose to?

A

Pneumococcus, Haemophilus, CEMA, PCP, giardia

186
Q

What pattern of infections do phagocyte defects predispose to?

A

Staph

187
Q

What pattern of infections do complement predispose to?

A

Neisseria

188
Q

What is the most common clinical picture associated with IgG subclass deficiency

A

Mostly normal

Next would be recurrent bacterial pulmonarysinus infections

189
Q

What immunoglobulin crosses the placenta?

A

IgG

190
Q

What’s the difference between conjugate and polysaccharride vaccine responses?

A

polysaccharide is T-cell independent and conjugate/protein is T-cell dependent

191
Q

what lymphocytes have receptor editing?

A

b cells

192
Q

what transcription factor is required for the development of regulatory t cells?

A

FOXP3

193
Q

recurrent neisseria immunodeficiency

A

complement

194
Q

recurrent meningitis complement deficiency

A

properdin deficiency

195
Q

What infection occurs in the absence of TLR3 signalling?

A

HSV encephalitis

196
Q

Defect in which complement pathway predisposes to lupus syndromes?

A

Classical pathway (C2, C1q, C4)

FRACP Shuyu (65 decks)

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