MT3 Session 12: Immune system and Vaccine Flashcards
2 WBC lineages of Innate immunity cells
myeloid, lymphoid
PMN leukocytes
myeloid WBCs:
polymorphonuclear - (lobed nuc) neutrophils - engulf
monocytes
myeloid WBCs:
nonlobed (norm) nucleus - macrophages and dentritic - engulf to present antigens on surface
natural killer cells
lymphoid WBCs- attack infected cells
B cells
lymphoid WBCs - mature in bone marrow
circulate; its plasma cells create anibodies and memory B cells
T cells
lymphoid WBCs - mature in thymus
helper T and regulatory T: regulate antibody response
WBC lineages: from hematopoetic stem cells onto
-Lymphoid : NK, B& T cells
-myeloid: PNM and monocytes
neutrophils, macrophages/dendritic
nonspecific host defenses
barriers - phys, chem
inflammation
phagocytosis
Toll-like receptors
- trigger cytokine release
2. recognize PAMP (pathogen-assoc molecular patterns) - things that pathogen classes (not species level) generally have
alternative complement pathway
structures LIKE LPS triggers a cascade that activates Membrane Attack Complex
pokes pores in target cell
antigen definition
anything that causes immune response, usually protein because more RIGID and VARIED in structure and ,so creates MORE SPECIFIC response
is a sum of epitopes
epitope
part of an antigen’s 3D structure or linear chain
the antigenic determinant - what one single antibody recognizes
activated antibodies (antigen bound) can trigger
complement cascade?
antibody structure
heavy/light chains, V/C
carboxyl/amino terminus
number of antigen binding sites/antibody
2
number of regions (V/C) in light/heavy
L: V L, C L,
H: Vh, Ch1-3
isotypes
Immunoglobulins A vs M GDE:
differences in heavy constant chains
idiotype, allotype
idiotype: differences in variable regions: enable to attach to different antibodies
allotype: person to person differences in constant regions, esp light chain - not normal classes
Primary&Secondary Ab response:
switch, decay
switch: at beginning, a high concentration to IgM switches to a high concentration of IgG
decay: sometime after the concentration of IgM is null, the concentration of IgG starts to decrease - will do so indefinitely if no secondary exposure
Primary&Secondary Ab response:
concentration of antibody isotypes
primary: increase in IgM, (switch) IgM decline as IgG increase to higher magnitude
secondary: even higher magnitude of IgG, almost identically magnitude bump in IgM
Is IgM a circulating antibody, mucosal, or cell surface?
circulating as pentameric
AND
cell surface (via Fc constant region in heavy end)
Is IgG a circulating antibody, mucosal, or cell surface?
circualting - major humoral response
humoral response
?
b cell receptor
Immunoglobulin (antibody) anchored to membrane protein of B cell
Clonal selection of B cells - mech
- IDENTIFICATION: antigen binds to a specific B cell receptor
- AMPLIFICATION: the whole B cell makes clones
- DIFFERENTIATION INTO i) plasma cells that release antibodies ii) memory B cells that can cause a rapid secondary response
what do B cells differentiate into?
plasma cells, memory B cells
generation of diversity of antibodies
IN B CELLS (for every variable region- 4 per abody):
DNA: join random D (diversity gene) with random V (variable region) gene
RNA: add 1 random J (joining) gene
add C region (mu or delta)
add other 3 chains
MHC
= major histocompatibility complex – make cell surface protein
contribute to female choice
how many Antigen presenting paths are there?
2: MHC I and II
MHC I Antigen presentation mechanism
- foreign protein in cytoplasm is degraded into segments
- segment brought into the ER to be attached to MHCI of ER membrane
- transport to golgi then to outer membrane
make B cells
MHC II Antigen presentation mechanism
- MHC chain in er becomes own vesicle
- microbe is phagocytosed and degraded to make antigens
- antigens and mhc fuse, put to cell surface
CD (4)
cluster of differentiation: cell surface protein on lymphoid cells
humoral vs. cell-mediated immunity
circulating antibody vs. kill infected cell
B cell activation: 2 routes, result
route 1: {antibody bind with antigen} + other antibody (2 dif characteristics of 1 antigen=substrate)-> make plasma (secrete IgM) and memories (higher affinity antibodies)
route 2: {abod and agen} bind withMHC of helper T cell-> (isotype switching) -> make plasma and memories
both make killers and B cells with same antigen binding site (SAME RESULT) - theres a redundancy and diversity
helper T cells (TsubH) function
bind with 1 B to create more plasma and memory cells
First vaccine: creator, vs. what?
Pasteur - vs. rabies
Polio: symptoms, characteristics
viral
attack nervous system, may impede breathing
what are the only countries that have endemic polio? why?
Afghanistan, Nigeria, Pakistan
small vocal minority attacks givers of vaccine because =spy? - CIA used an undercover doctor to confirm OsamabinLaden’s location
Strep Pneumoniae capsule function
niche: clingy so they aren’t blown away
virulence: protects vs. phagocytosis
Why is it hard to find a vaccine for Strep pneumoniae?
- they have a lot of capsule serotypes (about 100). we only found antis vs. 13
- they can switch serotypes by expressing a different kind they posses or by LTG
- there’s a selective pressure, so populations of (not the 13 known) increase
PCV13
pneumococcal conugate vaccine - 13 serotypes
gulf war syndrome is either caused by
oil fire - toxic
anthrax vaccine- and they were forced to geet it
what vaccine surrounds the autism controversy?
MMR - mumps, measles, rubella
MAC
membrane attack complex - what is activated to poke holes in alternative complement pathway
PAMP
pathogen-assoc molec patterns: what toll-like receptors bind to
