1.0 Immunology Flashcards
What occurs in reversible injury?
1) Cell swelling<br></br>2) Fatty deposits
Apoptosis vs necrosis
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Humoral vs cellular immunity
<b>Humoral</b> - antibody/complement mediated immunity<br></br><b>Cellular</b> - T cells (+ cytokine release)
Innate vs adaptive immunity
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What is the main haematopoietic organ?
Bone marrow
What are the primary lymphoid organs?
1) Bone marrow<br></br>2) Thymus
What are the secondary lymphoid organs?
1) Lymph node<br></br>2) Spleen
What are some lymphoid tissues?
1) Intestine<br></br>2) Tonsils (+ other mucous membranes)<br></br>3) Skin<br></br>4) Blood + lymph
What immune cells are lymphoid derived?
1) NK cells<br></br>2) B + T lymphocytes
What immune cells are myeloid derived?
<b>Granulocytes</b><br></br>1) Neutrophils<br></br>2) Eosinophils<br></br>3) Basophils<br></br>4) Mast cells<br></br><br></br><b>Monocytes</b><br></br><br></br><b>Macrophages</b>
What cells are the following CD proteins found on? (also what is their function?):<br></br><br></br>CD3<br></br>CD4<br></br>CD8<br></br>CD16<br></br>CD19<br></br>CD45<br></br>CD56
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What concentrations do cytokines work at?
10⁻¹⁰ - 10⁻¹⁵ M
Name four families of cytokines:
1) Interleukins<br></br>2) Chemokines<br></br>3) TNF<br></br>4) Interferons
What characteristics do all cytokines share?
1) Pleiotropism<br></br>2) Redundancy<br></br>3) Antagonism<br></br>4) Synergism
What is FAS ligand?
(FasL/CD95)<br></br>Member of TNF family<br></br>Trimer that binds to FAS receptor (CD95)<br></br>Causes apoptosis
What is perforin?
Monomer (similar to C9)<br></br>Aggregates → forms pores → allows ingress of <b>granzymes</b> → starts caspase cascade
What are the three kinds of innate immune recognition?
1) PAMPs<br></br>2) DAMPs<br></br>3) Missing self
What are the characteristics of PAMPs?
1) Shared by different organism classes<br></br>2) Molecular constituents essential for survival<br></br>3) Highly conserved<br></br>4) Not present in vertebral hosts<br></br>5) Allow discrimination between self and non-self
Give examples of PAMPs for:<br></br>1) Bacteria<br></br>2) Yeast<br></br>3) Viruses<br></br>4) Parasites
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Give 5 examples of PRRs:
1) Toll-like receptors (TLRs)<br></br>2) Lectins + scavenger proteins (MBL)<br></br>3) NOD + NOD-like receptors (NLRs)<br></br>4) RIG-like receptors (RLRs)<br></br>5) DNA receptors<br></br>6) Others (CRP)
What happens on activation of TLRs?
Activation → cytokine release → inflammation<br></br><br></br>Signal is via TIR domains<br></br>Activate NFkB, AP1 and IRF3 transcription factors
What are the ligands for the different TLRs?
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What is the mechanism of TLR4 action?
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How many types of NLRs are there in humans?
22
2) NLRP subfamily
2) Caspase 1
3) ASC
2) NALP3 activates caspase 1
3) Caspase 1 converts proIL-1β → IL-1β
IL-1β promotes inflammation
Molecules that initiate non-infectious immune response
Normal tissue can cause immune response if damaged by trauma/infection
- Heat shock protein
- HMGB1
2) Intracellular molecules
- ATP
- Uric acid
- DNA/RNA
3) Extracellular molecules
4) Non-self irritants
- Aluminium
- Silica
2) Phagosome fuses with granules from cytosol
3) pH of phagosome ↑ → killing bacteria
4) pF of phagosome ↓ → fusion with lysosome → complete degradation of bacterium
5) Neutrophil dies by apoptosis and is phagocytosed by macrophage
1) Activating receptor
2) MHC I inhibitory receptor
Presence of ligand at both → no killing
Presence of activatory ligand + absence of MHC 1 → killing of cell
Produced by cells with viral infections
These interferons interfere with viral replication and alert neighbouring cells and activate NK cells
Type 2 = IFN γ
Produced by activated NK cells
Activate macrophages
2) Calor (temp)
3) Rubor (redness)
4) Tumor (swelling)
5) Functio laesa (loss of function)
2) Dendritic cells
3) Mast cells
1) Bradykinin
2) Fibrin clot
3) Plasmin
- Vasodilation
- ↑ vascular permeability
- Pain
2) Fibrin clot
- Prevents spread of infection
3) Plasmin
- Breaks down clot
- Activates complement
1) IL-1α + IL-1β
2) IL-6
3) IL-12
4) TNFα
5) CXCL8 (IL-8)
- Pro-inflammatory
- Endogenous pyrogen (fever)
2) IL-6
- Pro-inflammatory
- Endogenous pyrogen (fever)
- Stimulates acute phase proteins
3) IL-12
- Stimulates NK + T cells →
i) ↑ IFN γ and TNFα secretion
ii) ↑ cytotoxicity
iii) ↑ Differentiation into Th1
4) TNFα
- Stimulates acute phase proteins
- Endogenous pyrogen (fever)
5) CXCL8 (IL-8)
- Attracts neutrophils
This is a lectin that binds carbohydrates
Allows rolling and slowing down of cell
Integrin
This is an adhesion molecule (binds to ICAM-1)
Allows cell to stop, adhere and transmigrate
2) Macrophages secrete TGFβ → ↓ inflamm.
3) IL-10 (from monocytes) → ↓ inflamm.
4) Lipoxins (from arachidonic acid) → ↓ inflamm.
5) IL-1R antagonist
6) Pro-inflamm. cells die by apoptosis
May have necrotic core
Lost of macrophages (histioctytes) - may fuse to become giant cells (multinucleated)
Granuloma is surrounded by:
1) Epitheloid macrophages (shoe sole shaped nuclei)
2) ECM (collagen)
3) other cells (lymphocytes, neutrophils + fibroblasts)
2) Opsonisation
3) Lysis of target cells
Small
Causes anaphylaxis
Activates/recruits phagocytes
C3b
Larger
Thioester bond
Susceptible to nucelophilic attack
(including factors that allow host cells to escape complement activation)
Properdin (Factor P)
Inhibited by
Factor H
Factor I
DAF
MCP
Especially Neiserria (gonorrhea + Neisseria)
C5a also recruits neutrophils
MASP-2 : C4 to C4a + C4b
C4b: C2 to C2a + C2b
C4bC2a = Classic convertase (Converts C3 to C3a + C3b)
Recruits C1
Results in cleavage of C4 - C4a + C4b
C1r (serine protease)
C1s (seine protease)
2) Opsonisation
3) Complement activation
1 x constant
1 x variable
Heavy chain
1 x variable
3 x constant (IgA, IgG, IgD) or 4 x constant (IgM, IgE)
2) Selection of different V, D, J segments
3) Junctional diversity
4) Somatic hypermutation
(also FcεRI mediates IgE-Eosinophil interactions)
MHC II = 13-25 peptides long
What are the different MHC class II isotypes?
HLA-A , HLA-B, HLA-C
Class II
HLA-DP, HLA-DQ, HLA-DR
2) Positive selection
2) Negative selection