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Innate Immunity Flashcards

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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

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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

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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
What kind of receptors do NK express?
activating and inhibitory
26
Stressed associated molecules
MICA MICB these are molecules on cell surfaces of stressed and infected cells
27
Activating Receptors (KARs)
recognize and bind MICA and MICB in NK cell
28
Protein Tyrosine Kinases in NK Cells
Engagement of activating receptors (KARs) triggers intracellular PTKs in NKs
29
Inhibitory Receptors (KIRS)
Class 1 MHC Molecules which are expressed on all cells in the body except RBCs
30
What does the engagement of KIRs do?
activated of intracellular tyrosine phosphatases (PTP) that negates the activation signal mediated by KARs in the steady state
31
What happens if both KAR and KIR are on?
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
What happens if only KAR is on?
NK cell activated and killing of infected cell | the MHC 1 is not expressed = no binding
33
How does NK cells kill target cells ?
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
Viruses
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
Explain the infection of Corona Virus
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
How does IFN-alpha/beta impact responses to viral infection?
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
How do PAMPs and DAMPs impact the viral infection response?
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
Describe the onset of Acute Phase Response and the sentinal cells involvement in this viral infection response
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
Which cytokine impacts fever the most
IL1
40
Which cytokine induces acute phase proteins the most
IL6
41
Which cytokine impacts arthralgia/myalgia
TNF-a
42
Describe the interaction of DCs in the immune response to viral infection
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
Describe the significance of Naive B Cells in Immune Response to Viral Infection
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
Describe the significance of Educated B Cells in Immune Response to Viral Infection
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
Explain the work of CD8+ in the Immune Response to Viral Infection
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
What does IFN-gamma do
plays important role in activation of Phagocytosis by tissue macrophages
47
what are the two principal pathogenic mechanisms of extracellular bacteria on infection?
inflammation: tissue destruction at site of infection bacterial toxins: virulent factors trigger diverse pathologic effects
48
Endotoxin
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
Exotoxin
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
CRP
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
MBL
activates the lectin pathway of complement activation.
52
what activates the alternative complement pathway
activates by SPONTANEOUS HYDROLYSIS of C3
53
what happens after the MAC is formed in the complement path?
Complement activation leads to bacterial lysis | MACs make holes in cell wall - osmotic shock
54
C3b
OPSONIZATION | deposited on bacterial surfaces opsonizes the pathogen and facilitates PHAGOCYTOSIS by phagocytic cells.
55
Soluble C3a and C5a
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
What does increased blood flow and local edema feel like ?
itchiness and irritation
57
how to c5a and c3a impact the movement of leukocytes to site of bacterial infection?
they bind to the receptors expressed on inflammatory cells

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