HTHSCI 1DT3 Lecture Notes - Lecture 19: Dendritic Cell, Monocyte, Type Iii Hypersensitivity

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MODULE THREE
Introduction to immunity
Roles of the immune system:
Defence against pathogens (pathogen recognition, adequate immune response, terminating the
immune response)
Self-tolerance
Adaptation to new pathogens
Wound healing
Defence against cancer
Removal of cells that have died through natural processes
Barrier function:
Lysozyme in tears
Skin
HCl, gut enzymes, colonisation with microbiota
Cilia and mucus
1) Primary lymphoid organs = bone marrow = all immune cells develop here / some can develop elsewhere e.g.
T cells in the thymus
2) Secondary lymphoid organs = LN and spleen
i.e. B cells in the cortex; T cells in the medulla
3) Tertiary lymphoid organs = Mucosa Associated Lymphoid Tissue (MALT)
Antigens enter via microfold (M) cells, meet DCs at the sub-epithelial dome (SED) for presentation to T cells
Differences between innate and adaptive immune responses:
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Document Summary

Defence against pathogens (pathogen recognition, adequate immune response, terminating the immune response) Removal of cells that have died through natural processes. Antigens enter via microfold (m) cells, meet dcs at the sub-epithelial dome (sed) for presentation to t cells. Neutrophils, dendritic cells, gamma-delta t cells, nkt cells. Pamps e. g. lps, lipoproteins, peptidoglycan, flagellin, bacterial and viral na, single-stranded rna, mannose-rich glycans are recognised by prrs e. g. tlrs and nod-like receptors. Tlrs = transmembrane prrs of which there are 10 different types on dcs, epithelial cells and nk cells mount cytokine reposne to initiate adaptive immune system. Nod-like receptors = intracellular prrs which recognise bacterial mdp; mutations in crohn"s disease. Nod2/card15 is a genetic susceptibility locus in crohns which activates nfkappab signalling in response to mdp; polymorphisms affect ligand-binding domain. Innate response to extracellular pathogens mediated by monocytes and macrophages. Macrophages detect pamps and complement; the triggering of complement enhances phagocytosis.

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