Immunology Flashcards
(196 cards)
1
Q
Most common class of primary immunodeficiency
A
Antibody disorders
2
Q
What type of PID does bacterial infections suggest
A
antibody deficien
3
Q
What types PID gets infections with encapsulated organisms
A
complement and splenic function
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
5
Q
Primary immunodeficiency disorders with absent B cells
A
X-linked agammalobulinaemia and 5-10% of CVID
6
Q
How to test for functional antibodies
A
Response to polysaccharide or conjugated vaccination
7
Q
Clues to phagocyte defect
A
lung, bones, soft tissue
8
Q
Wiskott-Aldrich syndrome
A
Eczema, thrombocytopenia, immunodysfunction
9
Q
Ataxia-telangiectasia
A
Defect in the ATM gene (impaired DNA repair)
10
Q
DiGeorge anomaly
A
Chromosome 22q11
Thymic defect with cardiac, cleft palet, hypoparathyroidism
11
Q
Hyper-IgE syndrome (HIES or Job syndrome)
A
Eczema, skin abscesses, lung infections, eosinophilia and high serum IgE
12
Q
Primary lymphoid tissue (2)
A
bone marrow and thymus
13
Q
Secondary lymphoid tissue
A
Spleen, lymph nodes, mucosal lymphoid tissue
14
Q
What T cells does MHC II and MHC I turn on
A
MHC II CD4
MHC I CD8
15
Q
Positive selection in T cell production
A
Selective T cell receptors that weakly recognises the self MHC receptors
16
Q
What stimulates TH1
A
IL-12
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
18
Q
Purpose of TH2
A
Targets helminth/parasites
19
Q
What Thelper is associated with allergy
A
TH2 (through the production of mast cells)
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
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
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
23
Q
CRP function
A
innate immune system because it binds to pneumococcus
it arises in acute phase response
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
25
How does lipopolysacchariedes (LPS) signalling cause septic shock
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
26
Toll-like receptors function
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
27
Gram negative sepsis shock pathophysiology
toll-like receptors
28
C-type lectins and its role in HIV
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
29
Dectin-1 and dectin 2
major receptors for fungae
| directs APC to TH17
30
Intracellular PRRs
TLR
NLD - NOD like receptors
RLR
ALR
31
NOD-like receptors roles (4)
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
32
Role of inflammasome in gout
The crystals in gout get phagocytosed. They are recognised by inflammasomes. That turns on caspase-1 and then IL-1 causing acute inflammation
33
Inflammasomes in Familial Mediterranean Fever
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.
34
Crohn's disease and NOD2
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.
35
Acute phase response induced by 3 monokines
TNF
IL-1
IL-6
36
What do the 3 acute phase response monokines target
TNF
IL-1
IL-6
Acts on the liver
37
IL-1
Fever
| Stimulates IL-1
38
What blocks IL-1
anakinra
39
IL-2
T-cell expansion
40
what cytokine has a role in inducing a generalised anti-viral state of cellular metabolism i other cells
Type 1 interferons
41
What releases Type 1 interferons
Plasmocytoid dendritic cells
42
What detects DNA in cytoplasm
AIM2 inflammasome
| cGAS
43
What simulates inflammasomes
NOD like receptors
44
What does macrophages differentiate from
monocytes
45
What cells generate oxygen radicals
macrophages and neutrophils
| - they also fuse with lysosomes with antimicrobial enzymes and proteins
46
what does NADPH oxidase do
generate oxygen radicals to kill microbials
47
NETosis
neutrophils die by NETosis and extrude DNA webs that trap bugs
48
ILC - innate lymphoid cells
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
49
ILC-2 pathology
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
50
What are NK cells a subset of
ILC-2
51
What do NK cells do
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
52
Difference between NKs and T cytotoxic cells causing cytotoxicity
NK cells respond to a lack of MHCI
| T cytotoxic cells senses viral particles which are presented to the surface of the infected cell
53
chemokines
cytokines that direct the movement of leukocytes
| Released from tissue sites and bind chemokine receptors on leukocytes and govern leukocyte migration
54
What are the 2 receptors required for HIV to enter a T cell
CCR5 and CD4
| however it can later mutate to use CXCR4
55
adhesion cascade
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
56
Leukocyte adhesion deficiency
Defect in the integrins or deficiency of selections (cannot roll along endothelium)
Present with bad tissue bacterial infections (but with abundant leukocytes in circulation)
57
what band on protein electrophoresis represents antibodies
gamma band
58
light chain ratios in humans
2 kappa: 1 lambda
59
How many hypervariable regions are there in an IgG
12
60
IgG subclasses
IgG 1-4
61
What IgG has good blocking function
IgG4
62
What isotype crosses the placenta
IgG
| protects neonates for the first 6 months of life
63
function of IGA
protection of mucosal surface
64
what transports IgA
plgR
65
how does immunisation to tetanus work
by neutralising the toxin
66
neonatal immunoglobulins
Maternal IgG transported during gestation
Neonates make IgM first then
Neonatal then synthesizes new IgG
Lastly IgA?
67
Isotypes, allotypes and idiotypes
isotypes are different Igs (IgG, IgM etc)
Allotypes - differences in the constant regions
Idiotypes - variations in the antigen-binding region
68
where do NK cells develop and what does they come from
fetal liver
| ILC/common lymphoid progenitor cells
69
which antibody chain has diversity segments
Heavy chain but not light chain
They both have V and J
70
what is a marker in newborn for B-cell primary immunodeficiency
TRECs/KRECs
| (quantitivate PCR) for SCID
71
Pre-B cell receptor
heavy chain pairs with 2 surrogate light chain
sends signalling for further maturation
72
what antibody is the immature B cell
Immature B cell is derived from the Pre-B cell
It has IgM
73
What antibodies are on the mature B cell
IgM and IgD (same antigen specificity)
It is naive until it becomes antigen experienced
74
BAFF and APRIL
expressed on antigen presenting cells
BAFF promotes survival for B cells
Upregulates TLR
Promotes immunoglbulin class switching
Memory B celldifferentiation to plasma cells
75
What autoimmune diseases are associated with elevated levels of serum BAFF
autoimmune hepatitis, PBC, SLE
monoclonal antibodies: belimumab, atacicept, blisibimod
76
what are the mechanism action of belimumab, atacicept, blisibimod
inhibitor of BAFF and APRIL to reduce B cell survival and reduce autoreactive B cells in SLE
77
which locus does antibody class switching occur
In the heavy chain locus, not the VDJ region
78
What B cell does CLL derive from
memory B cells
79
absolute antibody of T cells
CD3
80
what does the TCR on Tcytotoxic attach to
TCR attaches to MHC I
81
Autoimmune regular (AIRE)
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
Autoimmune polyendocrine syndrome Type 1
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
which cells do somatic hypermutation occur
The v region in the immunoglobulin loci for B cells
84
What is the second signal in T cell activation
The APC produces B7.1 and B7.2 (CD80 and C86) which binds to CD28
85
What is delayed deactivation/T cell exhaustion
CD80 and CD 86 binding with CTLA-4 and turns off activated T cells
86
What drugs targets IL-2
Steroids
Calcineurin inhibitors (inhibits IL-2 induction)
stops T cell expansion
87
What interleukin is vital for generation and maintenance of regulatory T cells
IL-2
88
Autoimmune lymphoproliferative syndrome
```
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
What markers do Treg cells have
CD4+
CD25 (interleukin 2 receptor alpha chain)
foxp3 (master regulator of Treg cells)
90
Super antigens
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
what T helper cells drive neutrophil infiltration
Th17
92
Th1 secretes
IFN-gamma, TNF
93
Mendelian susceptibility to mycobacterial disease
Genetic deficiency to amount Th1 response
94
What Th cells is involved in the atopic pathway
Th2 cells
Makes IL 4, 13 which target B cells to make IgE
Makes IL5 which makes eosinophils
95
what Th cell has a pathogenic role in psoriasis
Th17
| IL17 inhibitors e.g. secukinumab, ixekizumab, brodalumab
96
what corrollates with disease activity in Allergic Bronchopulmonary Aspergillosis
IgE
97
What is early phase response drive by in allergen challenge (e.g. asthmatics)
Mast cells (steroid resistant)
98
Clinical manifestations from PIDs from lack of antibodies
Recurrent sinopulmonary and gut infections
Organisms: standard organisms that cause these problems
99
Lack of T cells clinical manifestations
Same as AIDs sx
- Fungi - mucosal candida (lack of Th17)
- Viruses
100
Lack of neutrophils clinical manifestations
```
High-grade bacterial infections
Fungal infections (systemic vs lack of T cells which is more just mucosal involvement)
```
101
Complement deficiency clinical manifestations
If lacking classical pathways, get lupus and other autoimmune diseases
If lacking terminal components - disseminated neisseria infections
102
X-linked agammaglobulinaemia (Bruton's agammaglobulinaemia)
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
What antibody deficiency is coeliac's disease associated with
IgA
- measure TTG antibody (which is a subset of IgA)
- That's why need to also measure IgA
104
How to treat IgA deficiency
No IVIG
Prompt ABx
Transfusion with IgA deficient blood
105
Hyper IgM syndrome
```
Lack of CD40 to CD40L signal (between B and T cell)
Fail to class switch
```
Onset 1-2 years
Recurrent respiratory infections
106
the activation and cleavage of which of the following early complement components is most likely to elicit an inflammatory response
C3
107
Why does complement not bind to self
Complement control proteins
108
C1 esterase inhibitor deficiency pathology
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
Classification of hereditary angiooedema
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
Causes of acquired C1-inhibitor
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
Hereditary angiooedema C3/4 results
Reduced C4, normal C3
112
Treatment of hereditary angiooedema
1. Purified C1-INH protein
| 2. Bradykinin-2 receptor antagonistIcatibant
113
Complement deficiency associated with pyogenic infections
C3
114
Deficiency of complement regulatory proteins (CD59, CD55) causing red cells to be attacked by complement system
Paroxysmal Nocturnal Haemoglobinuria
115
PNH pathophysiology
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
Atypical HUS
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
Eculizumab
Monoclonal antibody against C5 and blocks further attacks of membrane lysis complex
Role in PNH
Atypical HUS
118
which chromosome is the MHC encoded
chromosome 6
119
HLA class I molecules
HLA-A, B, C
120
What cells do not have HLA I
RBC, some neuronal cells
| Higher expression on WBC
121
beta2 microglobulin
Reflects cell turnover, associated with poor prognosis for MM
Non covalent bond to long chain as a part of HLAI
122
HLA class II
DR, DQ, DP
On antigen presenting cells
123
Where does the CD4 bind to on the HLA II
Beta-2 domain
124
How many genes encode each of HLA II
2 genes per HLA - alpha and beta chains
125
HLA and drug hypersensitivity:
Abacavir
HLA B*57:01
126
HLA and drug hypersensitivity:
Carbamazepine
HLA-B*15:02 and HLA-A*31:01
127
HLA and drug hypersensitivity:
Allopurinol
HLA-B*58:01
128
What HLA does platelets express
HLA class I
129
Transfusion related acute lung injury mechanism
HLA antibodies from blood donor react against the patient receiving the transfusion
130
What are the 3 antigen presenting cells
Dendritic cells
Macrophages
B cells
131
TAP protein
TAP = transporter associated with antigen processing
They mediate peptide transport to eventually present the antigen on MHC I
132
Disease that inhibits TAP protein
HSV - stops antigen presenting
133
3 types of dendritic cells
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
Mechanism of immunotherapy for allergy
Small amounts of allergen leads to immune deviation to Th1 phenotype rather than Th2
135
Diagnosis of food allergy - role of skin prick
Rough correlation between size of wheal and likelihood of allergy
136
How often does childhood milk and egg allergy persist into adulthood
20%
137
Anaphylaxis diagnosis
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
Biggest predictor of poor outcome in anaphylaxis
Asthma
139
Diagnosis of venom allergy
Skin prick and intradermal testing
| but noted not for food
140
Mastocytosis
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
what anaesthetic medication can you not skin test
opioids because they are a natural mast cell degranulator
142
mechanism of ACE-I angiooedem
ACE normally breaks down bradykinin into an inactive metabolite
In ACE-I, there is defective bradykinin degradation
143
Chronic idiopathic urticaria duration criteria time frame
>6 weeks
144
Treatment for chronic idiopathic urticaria
Non-sedating H1 antihistamines (50% refractory)
No benefit in H2 antagonist
Omalizumab 300mg s/c q4weeks
Cyclosporine
145
Omalizumab
recombinant monoclonal antibody that forms complexes with free IgE to preventit from binding to mast cells
146
does bactrim and frusemide have cross-reactivity
unlikely because those allergic to bactrim are allergic to the specific antibiotic side chain (which is not present on frusemide)
147
Takayasu's arteritis - what kind of vasculitis and pathophysiology
Chronic inflammatory granulomatous aortitis
(Large vessel vasculitis)
Driven by T cells, IL-6
148
What viral infection is polyarteritis nodosa associated with
Hep B (also ass w HCV, HIV, hairy cell leukaemia)
149
Polyarteritis nodosa - type of vasculitis and pathophysiology
Systemic necrotising vasculitis of medium-sized muscular arteries
ANCA negative
150
Granulomatosis with polyangiitis (GPA) clinical sx
ENT, pulmonary, renal
ANCA +
151
Eosinophilic granulomatosis polyangiitis ANCA
ANCA only 50%, usually MPO >100
152
vasculitis associated with rapid progressive AKI (acute GN picture)
Anti-GBM
153
IgA vasculitis
Henoch Schonlein Purpura
154
Cold induced acrocyanosis + necrotic cutaneous ulcers
Cryoglobuinaemia
155
What is hyperacute rejection mediated by
Anti-A and anti-B antibodies
| Anti-HLA antibodies (from previous exposure to foreign HLA proteins)
156
Direct pathway in transplant rejection
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
Indirect pathway in transplant rejection
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
HLA matching in solid organ transplant vs haematopoietic cell transplants
HSCT requires better HLA matching to improve graft survival and reduce GVHD
-/12 match
159
GVHD mechanism + what prophylaxis is used
Donor T cells react against recipient tissues/organs
T-cell depletion
160
What does T-cell depletion in HSCT increase the risk of
Leukaemic recurrence
161
Mechanism of action of glucocorticoids as an immunosuppressant
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
Azathioprine
Stops clonal expansion of immune response as the metabolites are incoorporates into ribonucleotides - lymphocytes
Inhibits CTL/NK
Metabolised to 6-mercaptopurine and thioguanine
163
Calcineurin inhibitors
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
Mycophenolate
Affects leukocytes by inhibiting cell division through inhibition of IMPDH which is necessary for generation of guanine nucleotides
165
Methotrexate
Inhibits dihydrofolate reductase which decreases tetrahydrofolate and synthesis of thymidylate
Inhibits DNA synthesis
166
Cyclophosphamide
Alkylating agent and alters DNA
Affects Lymphocytes B>T and plasmas
167
Sirolimus
Inhibits mTOR
| Also binds to FKBP (like tac)
168
3 main inflammatory cytokines and their actions
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
Anti-TNF examples
Infliximab, adalimumab, golimumab
Etanercept
Certolizumab pegol
170
IL-1 examples
Anakinra
Canakiinumab
Rilonacept
171
IL-6 examples
Tocilizumab
| Siltuximab
172
Abatacept
CTLA4-Ig = B7 blocker
Prevents T-cell activation
173
Difference between ipilimumab and abatacept
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
Integrin blockers
Vedolizumab
| Natalizumab
175
What are mannose-binding lectin (MBL) and ficolin involved in
Lectin in the complement pathway
176
Chronic mucocutaneous candidiasis
Th17 deficiency --> failure to secrete defensins (a type of antimicrobial peptides - AMPs) --> candida susceptibility
177
How are toll-like receptors implicated in autoimmunity
TLR signalling in B cells can promote autoantibody formation
| May explain targeting of nucleic acid (ANA, dsDNA) in lupus
178
How does HIV from the mucosal surface get transported to infect T cells
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
What do inflammasomes do?
They sense PAMPs and DAMPs and activate caspase-1 and releases IL-1 (and less importantly IL-18)
180
What is released by the liver to prevent tissue destruction in the acute phase response
Alpha1-anti-trypsin
181
What do interferon type 1s do
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
RIG-I-like receptors (RLRs)
A type of pattern recognition receptors: detects viral RNA in the cytoplasm
183
AIM2/cGAS
Types of pattern recognition receptors that detected viral DNA in the cytoplasm
184
Which innate immune system cells are phagocytes
Macrophages (derived from monocytes)
| Neutrophils
185
What pattern of infections do B-cell defects pre-dispose to?
Pneumococcus, Haemophilus, CEMA, PCP, giardia
186
What pattern of infections do phagocyte defects predispose to?
Staph
187
What pattern of infections do complement predispose to?
Neisseria
188
What is the most common clinical picture associated with IgG subclass deficiency
Mostly normal
| Next would be recurrent bacterial pulmonarysinus infections
189
What immunoglobulin crosses the placenta?
IgG
190
What's the difference between conjugate and polysaccharride vaccine responses?
polysaccharide is T-cell independent and conjugate/protein is T-cell dependent
191
what lymphocytes have receptor editing?
b cells
192
what transcription factor is required for the development of regulatory t cells?
FOXP3
193
recurrent neisseria immunodeficiency
complement
194
recurrent meningitis complement deficiency
properdin deficiency
195
What infection occurs in the absence of TLR3 signalling?
HSV encephalitis
196
Defect in which complement pathway predisposes to lupus syndromes?
Classical pathway (C2, C1q, C4)
