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SFM > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Purpose of Innate Immune System

A

prevent, control, and eliminate infection without use of adaptive immune system

keeps infection in check until more specialized adaptive responses are activated

directs adaptive immunity towards either Ab-mediated or cell mediated response

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2
Q

Process of Tissue Repair

A

-Recognition host molecules related by stressed, damaged, and/or dead host cells
– Phagocytosis and clearance of cell debris
– Stimulation and control tissue remodeling

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3
Q

Circulating Effector Cells

A

Neutrophils
Macrophages
NK Cells

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4
Q

Neutrophils

A

early phagocytosis and killing of microbes

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5
Q

macrophages

A

efficient phagocytosis and killing of microbes, secretion of cytokines that stimulate inflammation

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6
Q

NK Cells

A

lysis of infected cells, activation of macrophages

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7
Q

Circulating Effector Proteins

A

Complement, Mannose Binding Lectin (collectin), C-reactive protein (pentraxin)

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8
Q

Complement

A

killing of microbes, opsonization of microbes, activation of leukocytes

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9
Q

Mannose Binding Lectin (collectin)

A

Opsonization of microbes, activation of complement (lectin pathway)

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10
Q

C-reactive protein (pentraxin)

A

opsonization of microbes, activation of complement

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11
Q

Inflammation Cytokines

A

TNF, IL-1, Chemokines

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12
Q

Resistance to Viral Infection Cytokines

A

IFN alpha and beta

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13
Q

Macrophage activation

A

IFN gamma

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14
Q

INF 12

A

Cytokine

INF gamma production by NK and T cells

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15
Q

IL-15

A

Proliferation of NK Cells

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16
Q

IL-10 and TGF Beta

A

Control of inflammation

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17
Q

Physical Barriers to Infection

A

Epithelial layers of skin and mucosal/glandular tissues

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18
Q

Chemical barriers to Infection

A

Acidic pH and anti-microbial proteins and peptides on surface

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19
Q

What mediates innate immune responses?

A

mediated by type I IFN (IFN-a/b) which render the anti-viral resistance to host cells and NK cells which kill virus-infected cells.

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20
Q

What mediates the adaptive immune responses?

A

mediated by CD8+ cytotoxic T cells (CTLs), which kill infected cells and complemented by production of Abs which block virus spreading.

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21
Q

Origination of NK Cells

A

Come from Lymphoid Progenator but are part of the innate immune system

Lymphoid progenitor –> Thymus –> T-cell precursor –> NK Cells

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22
Q

Function of NK Cells

A

recognize ligands on infected or stressed cells

induce APOPTOSIS on stressed/infected cells

eliminate reservoirs of infection by releasing intracellular pathogen for phagocytosis by tissue macrophages

NK cells must act in coordination with macrophages bc NK ONLY KILLS THE INFECTED CELLS BUT NOT THE VIRUSES THAT DID IT!

INF gamma released by NK prepares Macrophages to PHAGOCYTOSE viruses that have been released and thus PREVENT INFECTION of new adjacent host cells.
INF Gamma is important for activating tissue macrophages

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23
Q

IFN gamma/ IL-12 Amplification Loop

A

IL-12 induces IFN-Gamma in NK Cells
IL-12 is made by Macrophages
IFN Gamma activates phagocytosis and killing of microbes by macrophages
Macrophages treated with IFN- Gamma exhibit a CLASSICAL ACTIVATION

24
Q

Classical Activation

A

-increased synthesis of pro-inflammatory cytokines
-increased production of ROS (reactive oxygen species)
– synthesis of inducible NOS nitrogen oxidative species)
– up-regulation of lysosomal enzymes
– enhanced Ag-presenting properties

25
Q

What kind of receptors do NK express?

A

activating and inhibitory

26
Q

Stressed associated molecules

A

MICA
MICB

these are molecules on cell surfaces of stressed and infected cells

27
Q

Activating Receptors (KARs)

A

recognize and bind MICA and MICB in NK cell

28
Q

Protein Tyrosine Kinases in NK Cells

A

Engagement of activating receptors (KARs) triggers intracellular PTKs in NKs

29
Q

Inhibitory Receptors (KIRS)

A

Class 1 MHC Molecules which are expressed on all cells in the body except RBCs

30
Q

What does the engagement of KIRs do?

A

activated of intracellular tyrosine phosphatases (PTP) that negates the activation signal mediated by KARs in the steady state

31
Q

What happens if both KAR and KIR are on?

A

NK Cell is not activated and no cell killing

the ligand on the cell and the MHC Class 1 are bound to KIR and KAR

32
Q

What happens if only KAR is on?

A

NK cell activated and killing of infected cell

the MHC 1 is not expressed = no binding

33
Q

How does NK cells kill target cells ?

A
  1. NK cell releases perforins, which polymerize and form a hole in the enemy cell membrane
  2. Granzymes from NK cell enter perforin hole and degrade enemy cell enzymes
  3. Enemy cell dies by apoptosis
  4. Macrophage engulfs and digests dying cell
34
Q

Viruses

A

OBLIGATORY INTRACELLULAR MICROORGANISMs that use components of the nucleic acid and protein synthetic machinery of the host to replicate.

Viruses typically infect host cell types by RECEPTOR-MEDIATED ENDOCYTOSIS after binding to normal cell surface molecules.

35
Q

Explain the infection of Corona Virus

A

SARS-CoV-2 enveloped positive sense RNA viruses and they have Spike proteins that bind to ACE 2 on the host cell surface and fusion into the host cell

Corona virus infects and replicates amongst ACE 2 expressing epithelial cells

36
Q

How does IFN-alpha/beta impact responses to viral infection?

A

INTRACELLULAR VIRAL INFECTION

host cell activates via cytokine
it releases IFN alpha/beta which involves autocrine feedback loop -in which nearby infected cells in the tissue also respond

IFN alpha/beta inhibits viral gene expression and also increases expression of MHC1 molecules

MHC 1 molecules though hav e a viral peptide that is recognized by CTLs and then those CTLs bind and induce apoptosis in infected cells = cytotoxic T cells

37
Q

How do PAMPs and DAMPs impact the viral infection response?

A

Viral PAMPs and DAMPs activate tissue macrophages and dendritic cells

The activated macrophages release an array of cytokines and chemokines that mediate acute inflammation

Active dendritic cells engulf viruses and transport viral antigens to local lymph nodes via lymphatics –> activation of T cells follows
Soluble and specific viral antigens are transported by the lymph for activation of B cells in lymph nodes

38
Q

Describe the onset of Acute Phase Response and the sentinal cells involvement in this viral infection response

A

cytokines produced by sentinal cells (comprised of Macrophages and mast cells) upregulate the expression of adhesion molecules (P/E selectins and ICAM-1/VCAM-1)
Chemokines begin to attract leukocytes through the endothelium toward the area of infection
Cytokines IL1 ,TF alpha ,and IL6 are released by the tissue macrophage and enter the bloodstream to make systematic impacts

Fever, Acute Phase Protein induction, and Arthralgia/Myalgia

39
Q

Which cytokine impacts fever the most

A

IL1

40
Q

Which cytokine induces acute phase proteins the most

A

IL6

41
Q

Which cytokine impacts arthralgia/myalgia

A

TNF-a

42
Q

Describe the interaction of DCs in the immune response to viral infection

A

DCs are surrounded by T Cells in the Lymph Node
DCs present Antigens on their surface, in which the T Cell Receptors on CD4+ and CD8+ T cells can bind and become activated. These T cells become activated CD4+ Th1 or TH2 snd CD8+ CTLs

43
Q

Describe the significance of Naive B Cells in Immune Response to Viral Infection

A

Naive B Cells are independently activated by soluble/specific antigens which passively were brought in with the lymph flow
these B cells become activated (Ag-Activated B Cells) and produce low affinity/high avidity anti viral IgM Abs

44
Q

Describe the significance of Educated B Cells in Immune Response to Viral Infection

A

Th2 cells teach these B cells to differentiate and produce high affinity low avidity anti viral Abs IgG and IgA= EXACT SAME SPECIFICITY as the peptide that bound the DC and activated the CD4+

45
Q

Explain the work of CD8+ in the Immune Response to Viral Infection

A

Some CD8+ T Lymphocytes will recognize viral Ags (peptides) present on DCs
This activates the CD8+ cells into CTLS
The CTLs then leave the LN and move into peripheral tissue. CTLs look for infected cells which also have the antigen present on surface.
Bind to these cells and cause apoptosis

TH1 cells (CD4+) are important for CD8+ proliferation because they produce IL2

46
Q

What does IFN-gamma do

A

plays important role in activation of Phagocytosis by tissue macrophages

47
Q

what are the two principal pathogenic mechanisms of extracellular bacteria on infection?

A

inflammation: tissue destruction at site of infection

bacterial toxins: virulent factors trigger diverse pathologic effects

48
Q

Endotoxin

A

which are components of bacterial cell walls which are NOT
released by alive bacteria

ENDOTOXIN (LPS) of Gram-negative bacteria is a potent activator of Macrophages, DCs, and endothelial cells stimulating production of cytokines that cause disease.

49
Q

Exotoxin

A

Exotoxins also interfere with normal functions of host cells and stimulate production of cytokines that cause disease.
– Many exotoxins are cytotoxic. For example, diphtheria toxin shuts down protein synthesis in infected cells; cholera toxin interferes with ion/water transport; tetanus toxin inhibits neuromuscular transmission.

50
Q

CRP

A

an acute-phase protein in serum and interstitial fluid. CRP binds to microbial polysaccharides and LPS (lipopolysaccharides).

binding of CPR to bacterial substrates = classical complement pathway

51
Q

MBL

A

activates the lectin pathway of complement activation.

52
Q

what activates the alternative complement pathway

A

activates by SPONTANEOUS HYDROLYSIS of C3

53
Q

what happens after the MAC is formed in the complement path?

A

Complement activation leads to bacterial lysis

MACs make holes in cell wall - osmotic shock

54
Q

C3b

A

OPSONIZATION

deposited on bacterial surfaces opsonizes the pathogen and facilitates PHAGOCYTOSIS by phagocytic cells.

55
Q

Soluble C3a and C5a

A

CHEMOTAXIS

activate mast cells and mediate the CHEMOTAXIS of the blood cells into the injured tissue.

stimulate Mast Cells to release histamine to increase blood flow to the infected area

56
Q

What does increased blood flow and local edema feel like ?

A

itchiness and irritation

57
Q

how to c5a and c3a impact the movement of leukocytes to site of bacterial infection?

A

they bind to the receptors expressed on inflammatory cells

SFM (3 decks)

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