L1.3 Specific/adaptive immunity Flashcards
1
Q
What are dendritic cells
A
- Are Antigen presenting cells (APC)
- Senses/engulfs external particles → display foreign antigens on surface
2
Q
What are lymphocytes
A
- T-cells
- Helpers (CD4+) cytokines
- Cytotoxic (CD8+)
- B-cells → creates AB
3
Q
Features of asthma
A
- caused by sustained mucosal infections in the lungs
- Tissue damage & altered
- Mechanism:
- Dendritic cells pick up allergens → T2 cells → B cells (which produces IgE - only in asthma) & cytokines → both stimulating inflammatory cells (mast/eosinophils)
- Causes tissues damage/S.M damage/attenuates repair
- IgG is normally made in place of IgE
- Dendritic cells pick up allergens → T2 cells → B cells (which produces IgE - only in asthma) & cytokines → both stimulating inflammatory cells (mast/eosinophils)
4
Q
What is the normal non-asthmatic immune response?
A
- Foreign material in airway → inflammation recruits neutrophils & lymphocytes; dendritic cells activated → leaves tissues into lymph node
- Dendritic cells presents antigens to T-cells (MHC 1 & 2) → Co-stimulates IL-2 and allows proliferation of T-cells
- Dendritic cells recycled back to tissues
- T-cells help B-cells produce antibody → bind & neutralise antigen
5
Q
What is the role of AB
A
- Neutralization of toxins
- Activation of complement: kill/ingest
- Opsonisation for macrophages
- (identify foreign particles for macrophages)
- B cell antigen recognition system
- Persistent protection (usually)
6
Q
What is the mechanism of dendritic cells in lymph nodes
A
- Capture foreign antigen & present on MHC surface → to T cell R. CD4/8 (which is randomly generated)
- T-cells determine magnitude of response
- As T-cells are randomly generated, they circulate in tight lymph node env to find correct match for presented antigen
7
Q
T-cell R (Th1 & 2)
A
- Th1 → for bacteria
- Goes wrong → Multiple sclerosis; Rheumatoid arthritis
- Th2 → Parasites
- Goes wrong → asthma
8
Q
How do diseases become chronic? (e.g. asthma)
A
- Innate starts asthma → Th2 pathway (for first few years of childhood) → ILC 2 expands
- ILC 2 don’t require normal activation - having innate properties
- Activated by PRR & [ILC2] usually low
- ILC 2 don’t require normal activation - having innate properties
- With ↑[ILC2] → simple tissue damage (i.e. inflammation…) releases cytokine activating factors (same as Th2 cells)
- Innate response now primes disease → becomes chronic
9
Q
CD8 cells
A
- CD8 cells have perforins & granzymes
- Perforin punch holes in
- Granzymes enter cells
- Proteolytic cascade → kill cells
- Usually MHC1 molecules send signals to prevent CD8 cells from killing it
10
Q
Mechanism of influenza
A
- Viral infection, antigens presented on MHC1 molecules (asthma on MHC2)
- TLR (within molecule) recognises viral infection
- interferon spreads to neighbouring cells
- turns off protein synthesis & ↑ anti-viral mechanism
- CD8 attacks infected cells
- CD8 apoptose afterwards (due to ↓interferon signals)
- Tm (t-memory cells) survive → trigger B-cells to have long term defense