innate immune system

macrophage function

internalisation, antigen processing, killing, cell signalling, repair

natural killer function

killing, cell signalling

neutrophil function

internalisation, extracellular trapping, killing, cell signalling

eosinohphil function

extracellular trapping, killing, cell signalling, allergic reactions

mast cell function

internalisation, extracellular trapping, killing, cell signalling, repair, allergic reactions

dendritic cell function

internalisation, antigen processing, killing, cell signalling, allergic reactions

t helper cell function

cell signalling, immune memory, repair, allergic reactions

cytotoxic t cell function

killing, cell signalling, immune memory

b cell function

internalisation, antigen processing, cell signalling, antibody production, immune memory

systems within the immune system

lymphatic system, blood

organs in immune system

bone marrow, thymus, lymph nodes, spleen

molecules in the immune system

antibodies, cytokines, complement

3 mechanical barriers to infection

skin, tight junctions, mucosal surfaces

how is skin a good barrier

surface is dead skin cells and bacteria - unideal environment for pathogen growth, dry - prevents growth, sebaceous glands produce fatty and lactic acid which can damage pathogens

how do tight junctions prevent infection

stops ingested antigens passing from contaminated food into the body

how do mucosal surfaces prevent infection

mucus traps microorganisms so they can be shed from the body

physiological barriers to infection - 4

low stomach pH, normal microbiota outcompete pathogens, antimicrobial peptides, lysozymes in tears and saliva

4 reasons why parasites are effective pathogens

can evade immune response, hook on so they aren't flushed, can burrow through skin, too big for phagocytosis

which cells are granulocytes

neutrophils, eosinophils, mast cells, basophils

which cells are phagocytes

neutrophils, macrophages, dendritic cells

which innate cells are lymphocytes

innate lymphoid cells - ILCs, natural killer cells

4 signs of inflammation

heat, redness, swelling, pain

1st stage of inflammation - tissue damage causes …

resident sentinel cells to release chemoattractants and vasoactive factors - causes local increase in blood flow and capillary permeability

chemotaxis in inflammation

neutrophils and phagocytes migrate to inflammation site

which substances destroy bacteria

phagocytes and antibacterial substances

5 stages in local inflammatory response

chemokine release, activation of clotting and complement factors. neutrophils secrete chemokines to recruit monocytes, phagocytosis of pathogens, macrophages migrate to tissue

which chemokines are released and why?

CXCL8/IL8 released from damaged endothelial cells, TNF released from macrophages to recruit neutrophils, histamine release from mast cells for vasodilation and vessel permeability

what do macrophages do when they migrate to tissue

secrete IL1 and TNF - recruit lymphocytes, monocytes and neutrophils

3 stages in systemic acute phase response

fever, leukocytosis, CRP production

why do we have a fever

speeds up phagocytosis

leukocytosis def

increased WBC production

c-reactive protein production function

binds to microbes and activates complement proteins to aid phagocytosis

what is the complement system

a group of ~35 serum proteins made in the liver - critical for defence against pathogens, esp. extracellular bacteria, links to innate and adaptive immunity

7 functional categories of complement proteins

initiators, enzymes, opsonins, anaphylatoxins, membrane attack proteins, complement receptors, regulatory proteins

how does the body sense infection

Innate immune system detects molecules from pathogens Pathogen Associated Molecular Patterns (PAMPs) using Pattern Recognition Receptors (PRRs)

steps in phagocytosis

bacteria have PAMPs and phagocytes have PRRs - bacteria attach to pseudopodia - bacteria is ingested - forms phagosome - phagosome fuses with lysosome - bacterium killed and digested by lysozymes - digestion products released by cell

2 killing mechanisms

oxygen dependent killing & oxygen independent killing

oxygen dependent killing

oxidative burst - produces superoxide and other toxic oxidants, acts as antimicrobial

oxygen independent killing

lysozyme - hydrolysis, defensins - peptides kill many bacteria