L1.3 Regcosing the pathagens Flashcards
2 immune systems
innate and adaptive systems
3 types of barriers
-mechanical, chemical, biologic
components of innate immune system (IIS)
humoral components like plasma proteins and cellular like WBCs
3 types of WBC
lymphocytes, monocyte and granulocytes
3 types of lymphocytes
T,B and NK cells
3 types of tissue cells
macrophage, MAST and dendritic cell
types of pathogens
bacteria, protozoan, worms, flukes, fungi, virusus
what do we have to regconsice pathagens AGs
pattern recognition receptors (PRRs)
scienctic name for antigens
pathogen associated molecular patterns(PAMPs)
which cells has a lot of PRRs
all tissue cells
what are TLRs
PPRs expressed on the surface of the phagoctyic cells
how many TLRs
6
how to recognise exposed nucleic acids from a pathogen
- the nucleic acid taken up inside
- TLR-4 recgonise the NA
what type of PRR can detect pathogenic sugars
CLR on the surface of the macrophages and dendritic cells
whats the cell response after TLR is bound to the pathogen
inflammation, interferon and adaptive immunity (get rid of infection )
pathway of inflammation activation
TLR triggers release of NFkB,
- triggers release of proinflammatory cytokines/chemokines
- triggers inflammation and releases IL1, IL6, IL8 and TNFa
what are interferon
molecules that inhibit viral DNA replication by stopping protein synthesis and degrading mRNA
signs of infection
PAMPS leads to pain, redness, heat and swelling
why does blisters have no infection
there was physical damage to tissue cells
- so there was some necrosis
what are DAMPs
damage associated molecular patterns
-they are danger signals
-
what DAMPs can be released
- mitochondria
- ATP
- histones
- nucleic acids
how is pus formed
enzymes released by neurcotic neutrophils
- promotes inflammation
role of NK cells
kill infected and cancer cells
how many set of receptors of NK cells
2
-inhibitory and activatory
how does NK cell recongise and not kill normal cell
NK inhibitory receptor binds to MHC class I on normals - stop signals from activatory receptors
how does NK cell recnoginse pathogenix cell
no MHC class 1 so the activatory receptor bind to a antigen on the pathogenic cell - NK triggered to kill it by inducing apoptosis
how does a dendritic cell get activated
pathogen and antigen taken up by the cell
- expresses peptide MHC complex on the surface
- gets activated and migtrates to where it meets T cell to present the antigen
- then T and B cells starts to proliferate
- this is adaptive immunity
what is complement system
part of IIS, helping ABs to kill bacteria by using proteins
what are complenment proteins
pro enzymes that has 2 fragment s
role of small fragment of Complement porteins
mediator of inflammation
role of large fragment of Complement porteins
activates the next proenzyme and binds to microbe surface
3 pathway of complement activation
-lectin, classical, alternative
when does all 3 complement activation pathways converge
to form C3 convertases for C3 and C5
what are the consequences of the complement system
opsonisation, lysis and inflammation
how does C3b help opsonisation
C3b bind to the bacterial wall
- C3b then bind to thr CR1 (complement receptors) on phagocytes
- triggers phagoctyosis
what is membrane attack complex
they bury themselves into the bacteria’s surface and cause holes. This cause lysis of the surface
actions of C3a and C5a
activate tissue mast cells and endothelial cells
- attract innate immune cells to the infection site
