immunology Flashcards
how does the skin contribute to preventing infection
composed of tight keratinised cells that are, has a low pH and O2 tension, secretes hydrophobic oils, lysozyme and antimicrobial peptides
how does mucous prevent against infection
lines body cavities in line with outside world (GI tract), traps bacteria, secretes antibodies
how do commensal bacteria prevent against infection
symbiotic with host, compete with fatty acids, produce toxins to other bacteria
describe the nature of the innate immune system
fast, non adaptive present since birth
what are the cells involved in the innate immune system
Macrophages, dendritic cells, NK cells, mast cells (neutrophils basophils, eosinophils)
what is the inflammatory response
increases body temp and attracts macrophages
describe the nature of adaptive immunity
slow, specific, from memory
describe macrophages
pink cytoplasm and kidney bean nucleus, develop from circulating monocytes, they phagocyte cells, reside in tissues, monocytes are precursors
describe dendritic cells
present in large numbers in tissues, are professional antigen presenting cells to T cells, phagocytes
describe natural killer cells
release cytotoxic molecules that kill infected cells by apoptosis, respond to MCH I
describe mast cells
reside in tissues, single nucleus, fight antibody-coated parasites, illicit inflammatory response by degranulation (histamine, TNF, IL)
how do innate immune cells recognise pathogens
pathogens express PAMPs and immune cells have receptors for his PRRs
what is the main function of phagocytosis, what are the main cells
to ingest and kill cells/ bacteria/ fungi. macrophages, neutrophils and dendritic cells
describe how phagocytosis works (up until debris release)
PRR recognises PAMPs, creates phagosome around target. fuses with lyososme (contains ROS) and kills pathogen, debris is released to EXC space
how do phagocytes ‘remember’ antigens
peptides from antigen are expressed on cell surface receptors MCH II
what else is released after phagocytosis
pro-inflammatory mediators TNFa
describe opsonisation
coating of pathogens in opsonins to aid phagocytosis
name some major opsonins
C3b, Fc of IgG, CRP
what happens to virally infected cells
release interferons (INFa/b), NKC’s can recognise
what happens when large parasites are present
too large to be phagocytosed, results in degranulation - pro inflammatory substances eg IFNy
what are the 5 types of leukocytes (WBC’s)
neutrophils, eosinophils, basophils, monocytes, lymphocytes
what are neutrophils for
initiation and upkeep of inflammation
what are the steps of transendothelial migration
margination of neutrophils to endothelium, bind to adhesion molecules and pass across endothelial by diapedesis. attracted to site of injury by chemotaxis, activated by PAMPs and TNFa
neutrophils kill pathogens in what 3 ways and what do they release
phagocytosis, degranulation, NETs - TNF when activated
how do neutrophils kill by phagocytosis
pathogens release chemokines, phagolysosomal or ROS-dependent killing which requires NADPJ
how do neutrophils kill by degranulation
release of anti-bacterial protein
how do neutrophils kill by NETs
activated neutrophils release intracellular structures that immobilise pathogens and facilitate phagocytosis