Immunology Flashcards
innate immune system
sentinel innate immune cells present in all externally exposed tissue detect DAMPs/PAMPs via TLRs to allow broadly-specific and consistent responses
DAMPs
damage associated molecular patterns
PAMPs
pathogen associated molecular patterns
(eg flagellin & lipopeptides)
Toll-like receptors
present in sentinel immune cells on surface and in vesicles/endosomes and bind PAMPs/DAMPs
Apoptosis (Immune)
triggered by NK/CTL (external) or DNA/mitochondrial (internal) signals
= cell shrinkage & chromatin condensation -> nuclear fragmentation & blebbing -> apoptotic body formation
Necrosis (Immune)
cell lysis caused by external (trauma, temp, ischaemia, NO, ROS, NK) or internal (viral) damage
= damage -> organelle/cell swelling, cell membrane ruptures, cell contents release (DAMPs)
innate immune response
sentinel cells produce inflammatory mediators in blood and surrounding tissue
- causes vasculature leakage, enabling immune cells to locate site of damage via inflammatory gradient
- complement proteins and antibodies bind microbes to neutralise and enable detection by neutrophils which phagocytose, and undergo apoptosis
- NK cells detect viruses/mutated cell surface structures, and release perforin and granzyme B to form pores causing apoptosis of infected cell
innate return to homeostasis
monocytes differentiate into macrophages which phagocytose complement/antibody-microbe complexes
- differentiate to produce IL-10, VEGG, TGFb to cease inflammatory actions and promote tissue repair
complement/antibodies
binds microbes to neutralise them and allows detection by neutrophils/macrophages
anti-inflammatory mediators
IL-10, VEGF, TGFbeta
adaptive immune response
defends against specific repeated threats
adaptive immune response activation
dendritic cells ingest proteins from pathogens and dying cells and process them into peptides, which are displayed on MHC complexes
DCs migrate to lymph node and present peptide-MHC complex to T helper and effector cells. T helper cells activate B cells.
B cells
exhibit specific antibodies, once antigen detected under go clonal expansion into
- antibody producing plasma B cells (amplification of response)
- memory B cells
antibodies
specialised proteins that recognise specific antigens
- contain a Fv region for specific recognition and Fc region for complement binding/Fc receptors on macrophages/NK cells
IgM
transient (allows detection of duration of infection)
governs initial recognition
IgG
longer-lasting specific antibodies, common drug target
IgA
antibody specific to GI and respiratory illnesses
IgE
allergic reactions
IgD/basophils
govern a different arm of allergic reaction that IgE
neutralisation
antibodies directly bind an antigen to block interactions
- IgM, IgG, IgA
complement fixation
antibodies bind complement to induce membrane attack complex, which forms pores in bacteria to cause death
- IgG, IgM
opsonisation
coating of pathogen with antibody and complement to increase recognition for phagocytosis
- IgG, IgM, + complement
antibody-dependent cellular toxicity
Recognition of IgG by NK cells causing perforin and granzyme B release to form pores and cause apoptosis
T cells
recognise peptide-MHC complexes to destroy pathogens (CD8/CTL) or help other immune cells (CD4)