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HDM Midterm 2018 > Intro to Innate Immunity > Flashcards

Intro to Innate Immunity Flashcards

(63 cards)

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1
Q

Characteristics of Innate Immunity

A
  • responds rapidly to the presence of microorganisms
  • not antigen specific, limited diversity
  • no immunologic memory
  • stimulate adaptive immunity
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2
Q

Skin

A

Mechanical: epithelial cells joined by tight junctions, longitudinal flow of air or fluid

Chemical: fatty acids, B-defensins, lamellar bodies, cathelicidin

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3
Q

Gut

A

mechanical: epithelial cells joined by tight junctions, longitudinal flow of air or fluid
chemical: low ph, enzymes, a-defensins, regIII, cathelicidin

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4
Q

Lungs

A

mechanical: epithelial cells joined by tight junctions, movement of mucus by cilia
chemical: pulmonary surfactant, a-defensins, cathelicidin

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5
Q

Eyes/nose/oral cavity

A

Mechanical: epithelial cells joined by tight junctions, tears, nasal cilia

chemical: enzymes in tears and saliva (lysozyme, histatins, b-defensins

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6
Q

Chemical Barriers to infection

A
  • fatty acids, lactic acids (sweat, sebum)
  • destructive enzymes (lysozyme and phospholipase)
  • acidic ph
  • surfactant proteins A, D
  • defensins
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7
Q

Normal microbiota

A

10^14 bacteria
perform physiological, nutritional, protective function

reduces the area for the bad bacteria!

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8
Q

Granulocytes

A

Eosinophils
basophils
mast cells
All: release of pharmacological mediators, combat multicellular parasites, major role in atopic disease

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9
Q

Neutrophils

A

Professional Killers
-come from the bloodstream (takes 1/2 hr)
selectin proteins help capture the neutrophils attention

FORM PUS

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10
Q

What activates Neutrophils

A

IL-1, TNF A, IL-8

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11
Q

Macrophages

A

derived from monocytes

-prolonged defense

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12
Q

M1: classical macrophages

A

induced by innate immunity plays a role in inflammation

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13
Q

M2: alternative macrophages

A

induced by IL-4, IL-13
play a role in tissue repair and control inflammation
SHUT DOWN INFLAMMATION

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14
Q

Macrophage Innate Immunity Function

A

phagocytosis
cytokine production
inflammation
wound healing

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15
Q

Macrophage Acquired immunity

A

Ag presentation
regulatory cytokines
Effecor cells
activated mac: have increased phagocytic activity, can activate Th cells more, and have more higher levels of class 2 MHC/HLA on cell surface

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16
Q

Intracellular Killing Mechanism

A

Microbes bind to phagocyte receptor –> phagocyte membrane zips up around microbe –> microbe ingested in phagosome –> phagolysosome

w/i phagolysosome (arg–> citrulline: makes NO), ROS ……killing of microbes

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17
Q

Oxygen Independent Intracellular killing

A

lysozyme
defensins
lactoferrin
hydrolytic enzymes

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18
Q

Oxygen Dependent Intracellular Killing

A

Lysosome contains myeloperoxidase…..which goes on to make oxygen radicals that kill microbes

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19
Q

Chediak Higashi Syndrome

A

autosomal recessive (LYST gene, microtubule defect inhibitiing fusion

  • partial oculocutaneous albinism
  • recurrent pyogenic infections
  • presence of giant granules in leukocytes
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20
Q

Dendritic Cells

A 
APC
express high levels of class II HLA/MHC and CD80
-capture Ag in tissues then migrate into blood or lymph----> circulate to various lymphoid organs where they present Ag to T cells
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21
Q

Natural Killer Cells: Innate Immunity

A

CD16+, CD56+
immunity against intracellular infections (esp viral) and cancer

cell killing and secretion of cytokines: perforins and granzymes induce apoptosis in target cell

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22
Q

Adaptive Immunity

A

principle mediator of ADCC: activating receptor IgG Fc

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23
Q

NK destruction of infected cells

A

-destroy bacteria, parasites, fungi, tumor cells, virus infected cells

makes cell commit suicide by having perforin proteins deliver an enzyme called granzyme B into target cell

Fas ligand binds receptor on target cell: apoptosis

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24
Q

Macrophage/NK cell support

A

reciprocal cytokine activation

active macrophage produce and secretes IL-12 which activates NK cells

activated NK cells produce/secrete IFN-Y which activates magrophages (become better killers)

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25
Why do NK cells not target healthy cells?
because they interpret a kill or dont kill signal on the target cell HLA/MHC Class I is the inhibitory ligand
26
Pathogen associated molecular patterns (PAMP)
molecules shared by various classes of microbes but not present on self -they recognize structures of microbes that are essential for survival and infectivity PAMP ligands bind to PRRs: induce intracellular signaling in the phagocytes leading to their activation
27
Damage associated molecular patterns (DAMP)
molecules released by stressed cells undergoing necrosis that act as endogenous danger signals to promote and exacerbate the inflammatory response
28
Toll Like Receptors
receptors w/ specificities for different microbial products - respond to both exo/endo Ag - mac, dendritic, neutrophils ALL rec. pathogens by the same PAMPS/TLR
29
Respond of binding to TLR
ligand binds to TLR - phagocytosis and production and secretion of cytokines - increased ROS (more killing) - increased cytoskeletal changes(migration into tissues)
30
What is an Inflammasome
its a signaling system that detects pathogens and stressors -assembles sensor (NLRP-3), adaptor and the inactive caspase into an inflammasome ------> activates the caspase----> expression of IL-1 results in production of IL-1, IL-8(inflammatory cytokines)
31
DAMPS (Alarmins)
non-infectious cell damage/necrosis radiation, surgery, burns, UV light, etc this is doctor-induced!!! lead to very large inflammasome recruitment
32
Whats a component
serum protein that is produced by hepatocytes - not antigen specific - activates immediately in presence of pathogen stimulates inflammation, facilitates antigen phagocytosis, and can lyse some cells directly TIGHT REGULATION
33
b fragment in C system
active complement component binds to the target near the site of infection except 2b
34
The a fragment in C system
anaphylatoxins diffuses from the site plays role in initiating a localized inflammatory response except 2a
35
Alternative pathway
protects from pathogens in the absence of antibody (slow, less efficient) ``` C3-C3b-iC3b identify and bind to non-self membranes -have low levels of sialic acid -bacterial cells walls, yeast cells walls, viral envelopes -bound C3b will remain active longer ```
36
Complement pathway
C3a (inflammation) --> C3b(opsonization/phagocytosis) --> C5a (inflammation) ---> lysis of microbe
37
Anaphylatoxins
C3A, C4A, C5A(highly inflammatory) - induce smooth muscle contraction and degranulation of mast cells/basophils....cause release of inflammatory mediators histamine and vasodilators - inc capillary permeability (more movement of antibody, complement, phagocytes, lymphocytes and fluid in the infected tissue)
38
What is opsonization?
its another way to recognize and respond to pathogens -phagocytes have membrane receptors for IgG and C3b ENHANCES PHAGOCYTOSIS up to 4000 fold
39
Cytokine Type 1
hematopoietin receptor family | majority of cytokines
40
Cytokine Type II
all interferons plus | IL-10, IL-20, IL-22
41
Cytokine TNF Receptor family
TNFs induce adaptors that lead to activation of caspase-8, apoptotic FAS
42
Cytokine G-protein
mainly chemokines
43
Why Fever??
hypothalamic response to cytokines | muscle and adipose cells alter energy mobilization to generate heat
44
Effects of fever
bacterial and viral replication decreased at higher temperature - Ag processing is enhanced - adaptive immunity becomes more potent - human cells become more resistant to (-) effects of TNF-a
45
Innate Anti-Viral State
Interferon A and B directly inhibit viral replication by degrading mRNA: which inhibits protein synthesis IFN-a: produced by leukocytes IFN-b: produced by fibroblasts
46
Functions of interferon in a viral affected cell
IFN a-IFN b induce resistance to viral replication in all cells - increase MHC class I expression and Ag presentation in cells - activate NK cells to kill virus-infected cells
47
TGF and IL-10
regulatory cytokines contraction of immune resposne anti-inflammatory properties TGF-B: allows for repair w/o reg immune cells in vicinity IL-10: secreted by macrophages, dendritic cells and Tregs
48
C-REACTIVE PROTEIN
functions in opsonization, complement activation most widely used indicator of acute inflammation used clinically to follow disease progress and response to treatment
49
Recruitment of Leukocytes
IL-1 and TNF: increase expression of P and E selectings on endothelium (1-2 hrs) binds, detaches, binds (rolling of leukocyte) results in leukocyte slowdown flatten on endothelium, chemokine recruites it through the endothelium
50
Acute Inflammatory Response
occurs immediately after trauma, tries to prevent spread of pathogen, minimize further damage, enhance repair and healing THREE PROCESSES!!!!!! 1) vasodilation 2) increased vascular permeability(TNF, IL-1, histamine) 3)emigration of leukocytes from blood to damaged area
51
Edema
brings plasma proteins into intimate contact with damaged area
52
Proteins in inflammatory exudate
- clotting proteins(prevents further loss of blood) - complement(destroy bacteria) - kinin cascade(vasodilation, inc permeability of blood vessels, stimulates PAIN) - fibrinolytic protein(degrades cloth=wound healed)
53
Resolution of inflammatory response
-macrophage type 2 clean up cellular debris PRR: scavenger receptors specialized cytokines: IL-10, TG-B (shut it down cytokines)
54
Systemic Inflammatory Response Syndrome
pathogenic over stimulation of the immune response non-infectious (DAMPS): SIRS ---> shock infectious: SEPSIS ---> septic shock
55
Innate Acute phase cytokines
IL-1, IL-6, TNF
56
IL-1, IL-6, TNF
- stimulate the liver to make yet more acute phase proteins including CRP, C' - anaphylatoxin C5a (C') - virtual storms that confuse the immune systems
57
defect in phagocytes
increased susceptibility to extracellular bacteria and fungi
58
defect in natural killer cells
increased susceptibility to viral infections: herpes simplex
59
Leukocyte adhesion deficiency
widespread pyogenic bacterial infections
60
chronic granulomatous disease
intracellular and extracellular infection, granulomas
61
G6PD deficiency
defective resp. burst, chronic infection
62
Myeloperoxidase deficiency
defective intracellular killing, chronic infection
63
Chediak-Higashi syndrome
intracellular and extracellular infection, granulomas

HDM Midterm 2018 (2 decks)

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