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What is the difference between innate and adaptive immunity?

Innate immunity is immediate in response to infection, using relatively non-specific defence mechanisms. It activates and orientates the adaptive immune response.
Adaptive immunity 'tailors treatment'


What is the innate immune response made up by?

-Physical barriers including skin and saliva
-Soluble proteins in the tissues and circulation e.g. complement and acute phase proteins
-Cellular components including neutrophils and macrophages
- Cytokines released by cells - IFN-gamma and TNf-alpha


How does the innate system recognise non-self?

Through pattern recognition receptors, which recognise altered cells, oxidised cells, oxidised membrane structures etc
In infections, patterns recognised are those conserved in non-human cells e.g. Pathogen associated molecular patterns (PAMPs)


What to Toll-like receptors (TLRs) do?

These are located on the cell surface and in walls of intracellular vesicles, particularly in macrophages and dendritic cells. They recognise a range of pathogen-associated molecules from bacteria and viruses
They activate other molecule to induce the production of PRO-inflammatory cytokines and chemotactic factors


What do NOD-like receptors do?

Act as intracellular sensors of bacterial infection. They're located in the cytoplasm of cells routinely exposed to bacteria e.g. epithelial cells of the gut, dendritic cells and macrophages


What are some of the consequences of production of Pro-inflammatory cytokines (e.g. IL-1B/IL-6/TNF-a)?

Activation of complement opsonization, phagocytosis, decreased bacterial and viral replication and initiation of adaptive immune response


What do levels of C-reactive protein tell you?

This is a pro-inflammatory acute phase protein, and an important opsonin, so levels of it rise with an infection
High levels of CRP therefore tell you the body is fighting inflammation


What happens to Neutrophils during inflammation/infection?

Neutrophils normally roll along a vessel's endothelium. During inflammation, stronger adhesion molecules are expressed on endothelium, anchoring neutrophils to vessel wall. They then extravasate, squeezing between endothelial cells and traverse the basement membrane. They then ride a chemokine gradient to the site of inflammation


What's the process of phagocytosis?

-Phagocyte receptors bind to microbial surface components
-Bound pathogen is internalised into a phagosome
-Pathogen is killed either by phagosome acidification or through fusion with lysosome
-Soluble debris undergoes exocytosis


What are the three major classes of innate phagocytes?

1. Granulocytes: neutrophils, basophils and eosinophils. Neutrophils are recruited early and die early
2. Macrophages
3. Immature dendritic cells


What are the main cells involved in adaptive immunity?

T cells
B cells
Plasma cells


When does adaptive immunity kick in?

After about 12 hours, at which stage it is properly primed.
It proliferates within 1-3 days, and the makes antibodies which recognise the extracellular pathogen.


How are T-helper subsets divided?

Based on the transcription factor they carry, which dictates their function


What does co-stimulation do to T-cells?

Acts as a mechanism to avoid auto-immunity


What does Tolerance do with T-cells?

Prevents auto-immunity
Central tolerance takes place in generative lymphoid organs - bone marrow and thymus, in which immature lymphocytes are either apoptosed or developed into regulatory T-lymphocytes (CD4+ cells only), if they recognise a self-antigen


What is the connection between B cells and antibodies?

Antibodies are only produced by B cells that respond specifically to one antigen


What are some of the effector functions of antibodies?

-Neutralisation of microbes
-Opsonization and phagocytosis of microbes
-Complement cascade activation


What are the two consequences for a B-cell that recognises self-antigen in bone marrow?

1. Receptor editing so that it expresses a new antigen receptor and can be sent out to peripheral lymphoid tissue
2. Apoptosis

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