Flashcards
2: Innate immune system
Cards in this deck (14)
- 1Components- eliminate pathogens and
- initiate an adaptive immune response - 2Specialised phagocytes- Neutrophils phagocytose pathogens, and then die
- Macrophages and dendritic cells phagocytose pathogens and present antigens - 3phagocytes jobs- kill microbes and take up cell debris
- recognise PAMPs and release cytokines
- present antigens activating B & T - 44 of PRRs- Toll-like receptors (TLRs)
- C-type lectin receptors (CLRs)
- Intracellular nucleic acid receptors
- Nucleotide oligomerization domain/leucine-rich repeat containing receptors (NLRs) - 5TLRs recognise LRRs (Leucine rich repeat)- External LRR (leucine rich repeat) domain recognises ligands
Ligand binding causes -- oligomerisation of receptor and clustering of TIR (Toll/IL-1 receptor homology) domains
- Signalling cascades to activate the transcription factors NF-kB, IRF3 and IRF7 - 6intracellular RNA receptors- MDA5 detects long double-stranded RNA (+ssRNA picornaviruses)
- RIG-I detects short dsRNA and RNA with a tri-phosphate at its 5’ end (influenza A -ssRNA) - 7after PAMP detection, transcription of- Cytokines to regulate the immune response (e.g. IL-6, TNF-a)
- Interferons to warn neighbouring cells of viruses
- Chemokines to recruit immune cells to the site of infection
- Antimicrobial peptides to kill pathogens directly
- Enzymes e.g. cyclooxygenase 2 (COX-2) to make prostaglandins - 8complement system pathways- classical (cp)
- lectin (lp)
- alternative (ap) - 9cp1. IgG or IgM binds PRR
2. conformational change exposing Fc region binding sites
3. C1 initiator binds complex of 18
4. A conformational change in a C1r subunit then converts it to a protease, and cleaves the other C1r and C1s subunits, starting the complement cascade. - 10lp 1. lectin binds carb PRRs 2. Mannose binding lectin (MBL) binds mannose and other sugars on the surface of Salmonella, Listeria and other bacteria3. MBL is associated with MASP proteins (MBL-associated proteases). MASP2 is structurally related to C1s, and can cleave C2 and C4
- 11ap 1. direct binding of C3b to microbial surfaces 2. a low level of spontaneous binding of a labile form of C3 initiates (tickover pathway)3. C3b generated by tickover is able to directly bind to a microbial surface, otherwise it is degraded
4. Alternative pathway C3 and C5 convertases are produced, leading to C5-C9 and MAC formation - 12Effector functions of complement - anaphylatoxins C3a, C4a and C5a promote inflammation by acting as chemoattractants for immune cells and by binding to complement receptors- membrane attack complex (MAC), made of C5b,C6, C7, C8, C9 which forms a pore in pathogen membranes
- opsonins C3b and C4b bind to pathogen membranes and promote phagocytosis - 13e.g. TLR PATHWAYlipoproteins/viral proteins biind TLR1-2 - p50/p65 transcription factor activated - IFN beta encoded - IFN migrates outside cell and binds its receptor - expresses genes for pathogen recognition and attack
- 14the interferon response https://www-nature-com.ezproxy.lancs.ac.uk/articles/nri3665 (2014)1. Mx proteins and PKR induced making cells resistant viral rep.
2. MHC1 expression increased
3. NKs, DCs and macrophages activated
4. induce chemokines to recruit lymphocytes
(Iwasaki & Pillai, 2014)
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- BIOL 321: Clinical immunology Flashcards on 2: Innate immune system, created by Jumael Zafar on 05/10/2020.
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- Jumael Zafar
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