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Multisystem 1st Half > immune response to infectious agents > Flashcards

immune response to infectious agents Flashcards

1
Q

innate vs adaptive immunity

A

in innate, thereis inhibition of infection by type 1 interferons and killing of infected cells by NK cells

in adaptive, there is killing of infected cells by CD8 CTLs(cytotoxic t lymphocytes) and neutralizing antibodies block virus binding and entry to host cells.

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2
Q

PAMPs

A

(pathogen associated molecular patterns) are microbe molecules that are recognized by TLRs the innate immune system (toll like receptors) and PRRs(pattern recognition receptors)
o PAMPs activate type 1 interferons (IFN-alpha and IFN-beta)

 Viral PAMPs = ssRNA, dsRNA, and uncapped RNA

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3
Q

PRRs

A

pattern recognition receptors

receptors on host cells that recognize viral PAMPs

TLRs 3, 7, and 8

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4
Q

how do type 1 interferons work in innate immune response?

A

PAMPs activate type 1 interferons (IFN-alpha and IFN-beta)
 Viral PAMPs = ssRNA, dsRNA, and uncapped RNA

Type 1 interferons then:
 Induce enzymes that inhibit viral replication
 Increase expression of ligands for receptors on NK cells
 Activate NK cells to proliferate and kill virus-infected cells (apoptosis)

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5
Q

how do NK cells function in innate immune response?

A

type 1 interferon causes differentiation of cytotoxic NK cells (they kill infected cells by inducing apoptosis)

o	Healthy cells express MHC1 which connects with NK cell inhibitory receptor(no apoptosis)
o	Virus-infected cells do not express MHC class 1 (inhibited by virus)  connects with the NK cell activating receptor

NK cell killing is done via
 Perforin and granzymes = granzymes enter through perforin holes  activation of caspases and apoptosis of cell

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6
Q

which immune response uses NK cells?

what do NK cells use to kill?

A

innate

NK cell killing is done via
 Perforin and granzymes = granzymes enter through perforin holes  activation of caspases and apoptosis of cell

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7
Q

innate immune system response to viruses vs intracellular organisms vs extracellular organisms

A

viruses –> type 1 IFN and NK cells

intra –> phagocytes and NK cells

extra –> complement and phagocytes

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8
Q

adaptive immune system response to viruses vs intracellular organisms vs extracellular organisms

A

viruses –> CD8 (CTLs) and B cells/CD4

intra –> CD8 and CD4(TH1)

extra –> B cells/Ig and CD4

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9
Q

what activates NK cells?

A

TYPE 1 interferons

IFNalpha, IFNbeta, TNFalpha, and IL12

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10
Q

CTLs

A

cytolytic (cytotoxic) T lymphocytes (CTLs) = CD8+ T cells

part of adaptive immunity

CTLs can kill using
 Perforin and granzymes
Or
 FasL (Fas ligand) – Fas receptor is on the virus-infected cell  Fas + FasL induces apoptosis

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11
Q

how do CTLs sense virus?

A

o Viral proteins are presented on MHC class 1 to TCR on CD8+ Tcells

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12
Q

do CTLs affect healthy normal cells?

A

no, target specific

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13
Q

Thelper and neutralizing antibodies in adaptive immunity

A

Neutralizing antibodies block virus binding and entry into host cells – virus cant bind to host cell receptors!
o CD4+ T helper cells also needed for immunity; IgG aids in neutralization, opsonization, and sensitization for NK killing, mast cells, and complement system

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14
Q

common intracellular pathogens

A

Mycobacterium tuberculosis
M. leprae
Listeria monocytogenes
Leishmania spp.

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15
Q

what causes the damage with intracellular pathogens?

A

host response!

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16
Q

3 components of innate immunity to intracellular pathogens

A

Phagocytes (neutrophils and macrophages)
NK cells
cytokines (IL-12 and IFN-gamma)

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17
Q

once PRR is bound, 2 things happen…

A

o Phagocytosis and Cytokine production

18
Q

phagolysosome mechanism for killing

A

Macrophage receptors that recognize microbial surface (PRRs on the macrophage) bind microbes

microbes are internalized by receptor-mediated endocytosis

fusion of the endosome with a lysosome forms a phagolysosome which degrades the microbe

19
Q

cytokine feedback loop

A

Activated macrophages secrete cytokines that stimulate NK cells

NK cell and macrophage form a synapse in which IL-12 and IL-15 activate the NK cell

NK cells proliferate and differentiate into effector NK cells that secrete IFN-gamma

IFN-gamma binds to its receptor on macrophages and activates them to increase phagocytosis and secretion of inflammatory cytokines

20
Q

adaptive immunity to intracellular bacteria consists of 3 components

A

T cells (TH1/TH2/CD40L)
IFN-gamma
macrophages

21
Q

TH1 (CD4) vs Nk cells

A

• CD4+ T cells that develop into TH1 effectors = are more effective producers of IFN-gamma; they take over from NK cells

22
Q

development of TH1 response in adaptive immunity

A

Naïve CD4+ T cell is activated by dendritic cell with co-stimulation by CD28 + B7

clonal expansion and differentiation into TH1 and TH2 effector cells + production of IFN-gamma, IL-4, and IL-5

The antigen presenting cell (dendritic or macrophage) produces IL-12 when its receptors for microbe products are activated

the IL-12 activated naïve CD4+ T cell and causes differentiation of TH1 effector cells

TH1 then produce IFN-gamma

activation of macrophages  microbes killed

23
Q

damage in etracellular pathogen immune response

A

due to their exo and endo toxins

24
Q

3 pathways of complement activation

order of activation?

A

classical
lectin pathway
alternative pathway

A –> L –> C

25
Q

complement activation

A

C3 is cleaved to C3a and C3b –>cleavage exposes thioester bond  binds to pathogen surface

26
Q

C3

A

o C3 is the most important complement protein!

highly concentrated in body, highly reactive thioester bond, and mediates binding to pathogen surface

27
Q

classical vs lectin vs alternative complement pathways

A

Classical - c reactive protein or Ab binds to specific antigen on pathogen surface

alternative - pathogen surface is condusive to complement activation

lectin - mannose binding lectin binds to pathogen surface

28
Q

what does complement do after bound to pathogen?

A

o Opsonization and phagocytosis
 C3b binds to microbe and attracts phagocyte  causes phagocytosis

o Stimulation of inflammatory reactions = C3a and C5a (from C5 proteolysis) recruit and activate leukocytes  leukocytes destruct microbes

o Complement mediated cytolysis = C3b binds and activates late components of complement  forms a MAC (membrane attack complex)  osmotic lysis of microbe

29
Q

how does IL1, IL6, and TNFalpha decreased pathogen replication?

A

fever!, phagocytosis, and complement activation

30
Q

what is required for both intracellular and extracellular immunity?

A

CD4 Th2 cells

31
Q

how B cells and antibody act in adaptive immunity to extracellular pathogens?

A

Antibody mediated opsonization

Opsonization of microbe by IgG

binding of opsonized microbes to phagocyte Fc receptors (Fc-gamma-RI)

Fc receptor signals activate phagocyte –> phagocytosis and killing ingested microbe

32
Q

Fc receptor (FcgammaRI)

A

on phagocytes

binds opsonized microbes which activates the phagocyte to ingest and kill microbe

33
Q

in the classical pathway of complement, _____ activates _____

A

antibody activates complement

34
Q

early classical complement pathway?

late classical complement pathway?

A

early = c3 –> c3a (inflammation) and c3b deposits on microbe to cause opsonization and phagocytosis

late = c5 –> c5a (inflammation) and formation of MAC –> lysis

35
Q

in extracellular pathogen adaptive immunity, ____ blocks the binding of toxin to cell receptors

A

antibody

36
Q

______ responses protect against worm/helminth infections

how?

A

Th2

TH2 cells produce IL4, IL10, IL5 –> IgE and IgG production –> mast cell degranulation and eosinophil activation

37
Q

eosinophil granules protect against helminths because they have 3 toxic components

A

eosinophil peroxidase
major basic protein
eosinophilic cationic protein

38
Q

eosinophil peroxidase

A

enzyme that poisons parasites and cells by catalyzing halogenation –> triggers histamine release from mast cells

39
Q

major basic protein

A

a toxic protein that poisons parasites and cells by triggering histamine release from mast cells

40
Q

eosinophil cationic protein

A

a toxic protein that poisons parasites; a neurotoxin

Multisystem 1st Half (23 decks)

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