immunology pt. 3 Flashcards
phagocytosis
removal of pathogen by phagocytic cell
- neutrophils + monocyte/macrophage
- ingestion/destruction of infectious agents
«_space;infectious agents
phagocytosis process
- chemotaxis
- phagocytes migrate in region of inflammation
> by gradient of stimulant products from parasite host tissue at site of injury - adhesion (broad recognition)
- TLR: PAMP
- C3bR:C3b
- FcR: Fc region of antibody bound to pathogen - response
- extends pseudopods that enclose cells/particles - phagolysosome
- lysosome fuse to form phagolysosome - destruction
- oxidizing agents + acidic enzymes - elimination
- debris = released by exocytosis to ECF + blood
phagocytosis subversion
inhibit recognition
1. proteases degrade C3a and 5a, «_space;chemotaxis
2. “ “ C3b, «_space;opsonization
- capsule: electrostatic repulsion
- toxins: leukocidins kill WBC -> PUS
inhibit response
1. cytotoxins + lipases poke holes in phagosomes
- allows intracellular growth
2. stop fusion of phagosome w/ lysosome
- allows intracellular growth
innate (non-specific) immunity inflammation, fever + septic shock
inflammation: rxn to noxious stimuli
molecular mediators = proteins made by phagocytes + lymphocytes
effective inflammatory responses isolates + limits tissue damage
- destroys damaged cells + pathogens
skin inflammation
splinter introduces bacteria (PAMPs) + tissue damage (DAMPs)
complement proteins (C3a+5a) alert mast cell of non-self
- mast cell releases tumor necrosis factor alpha (NFA)
PAMPs bind TLR + C3bR
- antigen binds antibody if late primary/secondary infection on macrophage
macrophages releases
- TNFA
- IL-1, 6, and 8
TNFA
> > vasodilation + permeability
allows an influx of plasma
- brings in extra proteins like compliment
tumor swelling
IL-1
travels to the hippothalamus
» body temp
>»_space; functionality of immune cells
> «_space;replication
IL-6
travels to bone marrow
stimulates hematopoiesis
» # WBC’s
IL-8
aids in»_space; WBC
Adaptive (specific) immunity func
ID specific molecules of specific pathogen + destroy pathogens that subvert innate sys
Adaptive (specific) immunity characteristics
- antigen-specific
- immunological responses to specific pathogen causing an infection
- recognition of specific molecules (antigens) of specific pathogen
> NOT BY PAMPS OR PRRS
- must be able to distinguish self from non-self (tolerance) - response = antigen-dependent
- must be induced by host exposure to pathogen - lag time between exposure to pathogen + max response
- not immediately ready
- primary kinetic response = slow, associated w illness - exposure results in immunological memory
- secondary kinetic response = rapid destruction of identical agent, improved response
- memory response = immune protection, basis for immunizations
cells of immune responses
lymphocytes = mediate adaptive immune responses
- B cells make antibodies
- cytotoxic (CD8+) T cells kill infected host cells
- Helper T cells (CD4+) help activate B + T cells
natural killer cells (NK)
- innate immune response
- help bridge innate + adaptive immune cells
- kill infected hosts
Adaptive (specific) immunity recognition
T/BCRs/antibodies
- each lymphocyte makes unique proteins that interacts w a antigen
- R on different lymphocytes are mode of different a.a. and antigen specificity
Adaptive (specific) immunity recognition: infectious agents
every infections agent has a unique set of antigens
- each antigen yields unique response
- antigens = species/strain specific
Adaptive (specific) immunity recognition: antigen (non-self) - antibody generator
epitope = fragment of pathogens ID by antibidy
large proteins, some polysaccharides + nucleotides, toxins
Adaptive (specific) immunity recognition: B cells
ID bind to antigen (pathogen) directly
major histocompatibility complex (MHC)
- host cell surface protein
- func as antigen-presenting molecules for T cells
- reflect protein comp in cell
> normal cells: MHC have “self-peptides”
> cells that have ingested foreign proteins/pathogens + cells infected make ‘foreign” particles that interact with/ MHC
- T ce;;s ID antigen only on MHC
MHC I
on surface of nucleated cells
displays endogenous antigen for protection against intracellular pathogen
cells targeted for destruction by Tc CD8 cells
Tc (CD8+) cells
TCR binds MHC w foreign antigens in MHC
ID antigen (peptide) presented by MHC I on infected cells
> cells target for destruction
express CD8 protein coR
- maintain contact w MHC
- no T cell func w/o coR binding
MHC II
on pro-APCs: B cells, macrophages + Dendritic cells (DC)
displays exogenous antigens that have been phagocytosed/endocytosed
interacts w Th, CD4 cells
pro-APCS ( DC, B macrophages)
determine
1. when immune response is initiated
2. type of immune response (humoral/cell-mediated)
humoral response (B + Th2 cells)
induced by exogenous antigens
- G + made outside
- cell activation
T independent B cell activation
when large molecules bind multiple epitopes crosslinking several BCPs
- activated B cells make antibody molcules that bind + tag antigen for disposal
- CD4 Th cell, IL-2 or clonal explansion
> limited memory + class switching
T dependent B cell activation
digest bound surface antigen
- presents antigen to Th2 cells
activated Th2 cells secrete type 2 cytokines
- activate B cells
- causes B cells to differentiate
- clonal expansion of B cell in antibody-secreting plasma + memory cells
> memory cells do not need T cells for reactivation
response: antibodies
soluble proteins that bind + tag specific pathogen for destruction
- comp: 2 identical light + heavy chains linked by disulfide bonds
- variable regions (Vr/h) ID specific antigen
> both arms of antibody bind identical antigen
> vary among different antibody making cells but are same on 1 cell
> affinity: chem + physical complementary between antigen + specific binding site
- constant regions (Cl/h) = identical w/n each antibody classes
> Fc region may interact w complement/cells
