FSII mod 2 Flashcards
phagocytes are and do what
- neutrophil, monocyte, macrophage, dendritic cell
antibacterial immunity and cell bacterial infections
FC gamma R3A (CD16A)
antibody dependent cell mediated cytotoxicity (ADCC).
NK cells for virus and tumor THIS IS APOPTOSIS
FC epsilon RI
HIGH AFFINITY ADCC with IgE and Eosinophil AND some IgG
Helminth death
FC epsilon RI and mast cells
Mast cells increase mucous, intestinal mobility, recruit inflame, secretion of IL5 leading to more production of eosinophils
- for microbes
FC epsilon RI and eosino
IgE bound by FC epsilon Rs on eosino leading to degranulation and release of proteins
Fab portion reacts with epitopes on helminth and FC region binds to receptors of eosino.
c3a,4a,5a
are NOT attached to cell surfaces and increase perm of blood vessels along with IgG and IgM
Involves mast cell, neutrophils, monocyte and macrophage
**3 and 5 do mast dell degranulation during IgE stim
c3b
s attached to surface. Bacteria is coated with it and IgG then brings it to FC gamma RI receptor to do lysosome
Neutrophil and macrophage
b cell class switch IFNy
IgG
b cell class switch Il4
IgE
b cell class switch TGF b
IgA
- esp in mucosa
describe MHC
heterodimeric glycoproteins composed to 2 noncovalently associated polypeptide chains and have a groove for peptide binding site
what has MHC class 2
Found on B cell, macrophage, dendritic cells and activated T cells thymus epi
cd4 differentiation Il 12
Th1
cd4 differentiation Il 4
th2
il 2 t cells
autocrine clonal selection
dendritic cells uptake antigen
VIRUS uptake antigen via macropino and phago and MHC strongest on lymph tissue. FOR PROTEIN ANTIGENS
MACROphage uptake antigen
BACTERIA uptake antigen via phase, MHC can be induced by bac. FOR CELL MEDIATED RESPONSE
b cells uptake antigen
antigen uptake unique since endocytosis, cut it and present to CD4 ALSO activates itself. FOR HUMORAL IMMUNE RESPONSE TO CD4
antigen processing and presenting MHC class 2
XCELL endocytosis to phagolyso then presented to CD4 cell
antigen processing and presenting MHC class 1
mostly intracell and in proteasome already then presented to CD8
- self proteins, viral, intracell bac, fungi and parasites or tumors
th1 cells
- IFNY
activate macrophage and elim intracell path OPSONIN
Effector fun: antigen receptor, then APC cytokines and ligand interaction then IL2 to autoprolif then IFN y to class switch to IgG, macrophage activation and complement
Good for intracell bacteria that live in phagosomes of phagocytes!!!
They stim the phagocyte to kill the bacteria itself, no two signals needed.
After, it also increase expression of moles for T cell activation, secretion of inflame cytokines to bring in more WBC
- TB CELLS and the granuloma!!!! and delayed hypersensitivity
th2 cells
Il4 and 5
phagocyte independent immune fins
Effector fun: HEMLINTHS/incell paths
Il4 to stim macrophage for TISSUE REPAIR, make mucous and move intestine AND class switch to IgE and mast cell degranulation
Il5 for eosinophils
th 17
incude inflam, make antimicrobial peptides aka defensins.
treg
Maintain tolerance against self when bad T cells get OUT of 1 organ
types of rejection + what blocks it
Hyperactive: min to hr
Acute rejection: CD4,8 NK. 10-30 days
Chronic reject: months to years
cyclosporine will block t cell cytokine Il 2 so no reject
Leads to gingival overgrowth
Microbe immunity innate
epi barrier, phagocytes, dendritic cells, mast, NK, complement
microbe immunity adaptive
B lymph and antibodies, t lymph
XCell bac infections
B cells: neutralization, opsonization and Fc mediated phase, phase of C3b coated bac, inflame, lysis using mem attack complex
APC activate CD4 then release cytokines like IFNy and IL 17 so inflame, macrophage activation, antibody response
incell bac infection
innate: neutrophils, macrophage, NK cells
Adaptive: cd4 cells then macrophage via IFN y then kills bac in phagolysosome then cd8 comes and kills macrophage
virus mech
innate: block binding of virus to cell, OR NK cell kills infected
Adaptive: B cell neutralizes so virus can’t get in OR cd8 kills infected
parasites and protozoa
Th1 cells for ones that reside in macrophage *cell mediated)
Defense against infection is th2 leading to IgE and eosinophils
Cell interstitial spaces, blood lymph: viruses, bac, protozoa, fungi, worms
immune: antibodies, complement, phagocytosis, neutralization. This is humoral immunity
Th2 + th1
MHC class 2 on B cell + makes antibodies
epi surfaces infected
antibodies like IgA esp, antimicrobial peptides aka defensins
intracell cytoplasm infection
NK and cytotoxic t
MHC class 1
intracell vescicles
th1 cell and NK cell dependent macrophage activation
MHC class 2 on infected macrophage
- binds MHC2 with cd4 cell then release INFY to stim macrophage and use cd8 to kill macrophage apoptosis
IL1b cytokine
activates endothelium
tnf a
increases vascular perm + endothelium
IL6
wbc activation
- make acute phase proteins like mannose binding lectin, fibrinogen and c reactive protein
il 8
chemotactic, recruits neutro
il 12
Nk activating
who makes defensins
Usually cationic proteins made by epic, neutrophils, alveolar macrophage and found on mucosa. Puncture cell walls
tlr2
works with 1 and 6 for LTA
tlr4
dsRNA
tlr7
ssRNA
tlr9
CpG DNA
damps
sense self trauma.
Nucleic acids, histones, heat shock proteins (released OUT)
Work with TLR4 especially
soluble pattern recog molec
pentraxins, collecting and ficolins
Detect unique carb motifs on bac, fungi and virus and also damaged self
Collections can activate complement
They cluster the microbes and neutralize, opsonin, inflame, complement on, interact with FCy and cytokine (pentraxins)
Pentraxin PTX3: is predecessor of antibody!!! Ante antibody and have same functions
how do neutropjhils killc ells
superoxide anion through oxidative burst of cell
ILC
Innate lymphoid cells
ILC are lymphocytes but No t or b antigen receptors!!!
Found on barrier surfaces where they regulate immunity, infram and tissue repair
Immune tolerance to gut
ILC 1
or bac and virus for immunity against virus, intracell bac and parasites, tumors
- paired with TH1 since both make IFNy
ILC2
eosino helminths
th2 partner. both make IL4,5
ILC 3
IL17 then antimicrobial peptides for immunity against extracell bac and fungi
CD8 innate partner is
NK cell: both do INFy and perforin
interferons
made in response to inflame or infection
Type 1 or a/b: made by most cells like epic and fibroblasts
Resistance to viral rep, increase MHC1 in app and activate NK cells
IFNa and B
Basically tell cell that is NEXT to the virus infected cell to release antiviral proteins to degrade viral MRNA so virus can’t rep
Corona messed with this by stopping IFN
Innate
type 2 interferons
gamma; made by lymphocytes
Do host control of viral rep in COLDS and infections
NLRP3 complex
Signal 1: Nf- kappa B activation after detect something with TLR4 then increased expression of inactive NLRP3 and IL1B
Signal 2 is activation of NLRP3 then assembly of complex and cascade 1 on so turns on IL1b
activation of MAMPS/DAMPS, potassium efflux, lysosome damage, mito damage and endogenous damage
inflammasome
multiprotein complex that assemble in cytosol after exposure to MAPM or DAMP and activate C2 then cleave IL1B that is secreted
Mediate protection against infection and inflame
acute phase proteins
proteins in plasma that increase during infection and inflammation
Bacteria induce macrophage to make IL6 then make acute phase proteins like mannose binding lectin, fibrinogen and c reactive protein
C reactive protein binds phosphorylcholine on bac then opsonin and complement activated
Mannose binding lectin also opsonin and complement
cytokine storm
done by 5a
anti inflamm mech
IL 10 and TGFb made by macrophage and Treg
Downreg inflame, termination of neutrophil recruitment, clearance of apoptotic neutrophils by tissue phago, tissue repair
Efferocytosis
phagocytosis of apoptotic neutrophils by tissue macrophages
- eat me signal
Macrophages are reprogrammed and downreg proinflam cytokines and upregulate antiinflam
DEL1 protein physically links apoptotic neutrophils to macrophages BRIDGE and facilitates clearance of apoptotic cells
adaptive vs innate genetics
Adaptive memory
Is permanent genetic changes like gene recombination and somatic hypermutation
innate is epigenetic, rewiring chromatin NOT perm so lasts short
B glucan
major cell wall constituent of fungi and induces epigenetics + interacts with dectin 1 on macrophage
- cross protection thing
- tumors!!! BUT also can be hypertrained for inflammation and neutrophils leading to stuff
vaccines work using
innate immune memory and adjuvant!!
immunogenic epitopes
organic, proteins, size, complexity, charge, foreignness, mode of administration and genetic constitution
how many types of iga and g
2 iga and 4 igg
fc region
effector function of antibody is in heavy chain constant region
can calculate an ___ for antibody interaction
affinity constant
how can antibody be found
in plasma mem of b cell (antigen receptor), associated with fc receptor on cells or in sol form
ITAM and ITIM
a is activation, i is inhibition
mucosa antibody
dimeric IgA
epi + endo antibody
IgE
- NO ANTIBODY IN BRAIN
IgG function
complement, opsonization, adcc with nk cells and cross placenta
IgE function
basophil and mast degranulation, ADCC with eosino
neutralization of virusq
happens via blocking attachment at receptor binding site
- antibody varibal regions Iga, M and G
features of mucosa
- interact with lymph in discrete compartments and has unique antigen uptake mech
what changes in class switch
b cells make 1 variable chain but in switch, changes its heavy chain constant region part
helminth immunity
- mast cells: increase mucous, digestive motion, recruit WBC< secretion of Il5 so more eosino
- IgE: bound to fcE on eosino leading to degranulation
- also a bit of IgG
t cell antigen receptor structure
a and b chains with constnat and variable regions and cd3
cytotoxic t cell diff
0 CD4 helper can produce cytokines with APC so costim
- CD4 can enhance ability of APC to stim cd8
- if apc is directly infected or has phago a path, can stim without cd4
primary vs secondary humoral immune response
- primary is Igm
- secondary is IgG, A or E and stronger more specific response
antibody structure
- 110 aa are variable
- remaining 110 and 330 are constant
- carb side groups increase sol, stop degredation and enhance fc domains
what stops rolling neutrophi9l
pentraxin 3 binds endothelial p selectin
what stops chemokine induced activation of b2 integrin
aka LFA1
- growth diff factor 15
what stops firm adhesion of neutrophil
endothelial del 1 binds lfa1 to stop adhesion
how do neutrophils enter tissue
rolling adhesion then tight binding of LFA 1 on neutro and iCAm on endo
- diapedesis
- if CD18 mutation then less LFA1 and less neutrophil in infected areas
prrs vs t cell receptor genetics
prr are encoded in germline where t cell receptors and b cell are generated randomly by gene recombination
antibody vs t cell infection moderation
b cells do extracell. t cells do intracell
bacteria involve
macrophage, dendritic cell, neutrophil
virus involve
dendritic cell, neutrophil
parasites involve
neutrophil and eosino
c5 to 9
is NOT apoptosis!!!
what allows cd8 to bind class 1 and cd4 to bind class 2
cd8 can bind polymorphic and non
- cd4 can onl6 do nonpolymorph
whats in inflammasome
Consist of : cytosolic PRR (NLR) protein that detects DAMPs/PAMPS
Adaptor protein ASC
Cascade 1 (or procaspase inactive)
inflammation on vascular endo
vasodilation, adhesion molec, loosen cell junctions (tight) and clot microvessels
dna vs histone meth
dna meth is always off , which histone meth depends on situation
key reg mech of trained immunity
TCA (fumerate and acetyl coa), chromatin, gene expression
- same mech in worms lol
