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Immunity > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Opsonization

A

Coating a microbe with molecules that can be recognized by receptors on phagocytes

Ex. IgG expressed on microbe, IgG binds to receptors on phagocyte, crosslinks

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2
Q

Phagocytosis (4 steps)

A
  1. Fc receptors on phagocyte bind to opsonized microbes
  2. Fc receptor signals activate phagocyte
  3. Phagocytosis of microbe
  4. Killing of ingested microbe
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3
Q

Role of immune system (4)

A
  1. Defense against infection (vaccinations boost immune defenses)
  2. Defense against tumors (immunotherapy for cancer)
  3. Injure cells; pathologic inflammatory response (cause of allergic, autoimmune, inflammatory diseases)
  4. Recognizes and responds to tissue grafts and newly introduced proteins (barriers to gene therapy and transplantation)
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4
Q

Principles of Innate Immunity

A

Inflammation or antiviral defense

  1. Present in healthy individuals at birth
  2. Receptors are encoded in germline
  3. Restricted response without memory**
  4. Immediate
  5. Physical and chemical barriers (1st line of defense)
  6. Enhances adaptive immune responses
  7. Response similar to repeat encounters with an infectious organism
  8. Able to recognize and respond to invariable (nonchanging) structures
  9. Does not normally react against host
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5
Q

Innate Immunity Defense (at site of microbial entry)

A

GI tract, epithelium, resp. tract

Physical barrier, antimicrobial molecules, lymphoid cells

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6
Q

Innate Immunity Defense (at tissues where microbes breach)

A

Macrophages, dendritic cells, mast cells (secrete cytokines)
Initiation of inflammation

Phagocytes destroy microbes and then eliminate damaged cells

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7
Q

Innate Immunity Defense (in blood)

A

Plasma proteins complement microbial destruction

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8
Q

Innate Immunity Defense (for Viruses)

A

Induce production of interferons from infected cells to inhibit infection of other cells

Through the production of Natural Killer cells (that kill)

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9
Q

Adaptive Immunity

A
  1. Specific or acquired
  2. Memory responses through somatic rearrangement of gene segments during lymphocyte development leading to clonal expansion of B and T lymphocytes
  3. Immune response:
    Expansion and differentiation of lymphocytes
    Adapts based on exposures and vaccines
  4. Develops later in life
  5. Lymphocytes (receptors) and immunoglobulins (antibodies)
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10
Q

Specificity (Innate vs Adaptive)

A

Innate: Structures shared by classes of microbes (PAMPs) or damaged cells (DAMPs)
Identical TLRs recognize different microbes

Adaptive: For structural detail of microbial molecules (antigens); may also recognize nonmicrobial antigens
Distinct antibodies recognize different microbes

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11
Q

Receptors (Innate vs. Adaptive)

A

Innate: Encoded in the germline; limited diversity
NOD-like receptors (cytosolic), mannose receptors, Toll-like receptors
Nonclonal (identical receptors on all cells of the same lineage)

Adaptive: From somatic recombination of gene segments; greater diversity
Clonal (clones of lymphocytes with distinct specificities express different receptors)

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12
Q

Microbial Recognition (Innate vs. Adaptive) and their interplay

A

Innate:
Recognize structures shared by classes of microbes that aren’t present on host cells
Enhanced function through adaptive immune system

Adaptive:
Lymphocytes express receptors (antibodies) on their cell surface that recognize specific antigens
–> Molecules present on microbe surface
–> Non-infectious substances that are involved in a microbial infection
Utilizes cells of innate immunity (phagocytes) to eliminate microbes

Antibody binds to microbe, which activates phagocytes (innate) to ingest and destroy the molecule

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13
Q

PAMPs

A

Pathogen-associated Molecular Pattern
Recognized by the PRR (innate)

Microbial molecules, shared by microbes of the same type
Not on normal host cells
Stimulate innate immune responses
Essential for survival/infectivity

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14
Q

DAMPs

A

Damage-associated Molecular Pattern
Recognized by the PRR (innate)

Released from damaged or necrotic host cells
Present in injury (infarction) or infection

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15
Q

Toll-Like Receptors (TLRs) (innate)

A

Specific for microbial components
Extracellular: lipids, proteins, polysaccharides on cell surface of microbe
Intracellular: nucleic acids of ingested microbes

Activate TFs to stimulate production of cytokines, enzymes, etc.
Ex. Nuclear factor KB (NFKB) promotes items involved in fighting infection

Defect in TLR signaling (recurrent or severe infection)

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16
Q

TLR Signaling Cascade (innate)

A
  1. TLR binds bacterial or viral molecule
  2. Recruits proteins to activate transcription
  3. NF-kB
  4. Increases production of cytokines, adhesion molecules, and costimulators
  5. Acute inflammation, stimulation of adaptive immunity

OR

  1. Interferon Regulatory Factors (IRFs)
  2. Increases production of type 1 Interferons (IFN a, B)
  3. Antiviral state (blocks viral replication in host cells)
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17
Q

NOD-like Receptors (innate)

A 
Family of cytosolic receptors that sense DAMPs and PAMPs in cytoplasm that contain:
Central NOD (nucleotide oligomerization domain)
Different N-terminal domains

NOD1 and NOD2
Contain N-terminal (Caspase Related Domains)
Bacterial peptidoglycans in the cell wall
Activated NF-kB

NLRP-3
Recognizes microbial products, substances associated with damage, and endogenous substances in large quantities (crystals)
Enhances production of IL-1bB (inflammation, fever)

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18
Q

Inflammasome

A
  1. NLRP-3 oligomerizes with inactive caspase-1 inflammasome
  2. Activated caspase-1 cleaves IL-1B precursor (coming from nucleus after innate signals enhanced production of pro-IL1B)
  3. Activated IL-1B generates fever

Inflammatory dysregulation:
Gout: urate crystal deposit
Autoinflammatory syndromes

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19
Q

Components of Innate Immunity (10)

A
  1. Epithelial barrier
  2. Phagocytes: neutrophils and monocytes/macrophages
  3. Dendritic cells
  4. Mast cells
  5. Innate lymphoid cells
  6. Natural Killer cells
  7. Lymphocytes with limited diversity
  8. Complement
  9. Plasma proteins
  10. Cytokines
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20
Q

Epithelial Barrier

A
  1. Mechanical barrier of tightly adherent cells
  2. Produce mucous
  3. Chemical barrier of peptide antibiotics (defensins and cathelicidins)
  4. Intraepithelial lymphocytes: limited diversity, function is not well known

Barriers to infection and presence of microbial killers (local antibiotics and intraepithelial lymphocytes)

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21
Q

How do leukocytes get to where they need to go? (5)

A
  1. Rolling
  2. Guided to epithelial barrier by selectins which slow the cell down
  3. Integrins activated by chemokines bind to the cell via ligands to the epithelium
  4. Stable adhesion
  5. Migration through endothelium

Integrins are what directly cause binding for diapedesis

Once inside the tissue, chemokines direct to area of infection
Cytokines at infected area promote more recruitment to area of infection

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22
Q

Neutrophils (phagocytes)

A

[Polymorphonuclear leukocytes (PNMs)]

  1. Most abundant leukocyte in the blood
  2. Increase rapidly during infection (cytokine simulation
  3. First cell to respond to infections (bacterial and fungal)
  4. Dominant cell of inflammation
  5. Phagocytose microbes in the blood and tissues and destroy them
  6. Recruited to tissues to remove debris
  7. Live for only a few hours in tissues, dead ones form pus
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23
Q

Band neutrophil

A

Immature neutrophils

Can be released when they’re immature because the stimulation is so intense

Indicative of an overwhelming infection

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24
Q

Oxidative (Respiratory) Burst and ROS toxicity to microbes

A
  1. Microbe is recognized by PRRs and phagocytosis occurs
  2. Membrane closes around microbe, forming a phagosome
  3. Phagosome fuses with lysosome forming a phagolysosome
  4. Phagocyte oxidase converts molecular oxygen into ROS
  5. ROSs are toxic to microbes and work with inducible nitric oxide synthase (iNOS) and lysosomal proteases to destroy microbes
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25
Q

Monocytes/macrophages (phagocytes)

A
  1. Monocytes differentiate into macrophages in tissues
    Brain: Microglial cells
    Liver: Kupffer cells
    Lungs: Alveolar macrophages
  2. Found in all connective tissues and organs
  3. Survive very long in tissues
  4. Ingest microbes in blood and tissues
  5. Clear dead tissues
  6. Initiate tissue repair
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26
Q

Macrophages

A
  1. Cytokines regulate and induce inflammation
  2. Phagocytose microbes because of recognition on cell surface receptors
  3. Activated by PRRs (TLRs and NLRs)
  4. Clear dead tissues
  5. Initiate repair process
  6. Some phagocytic receptors activate killing
  7. Respond to cytokines
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27
Q

Macrophage activation (classical vs. alternative)

A

Classical:

  1. Monocyte (with TLR ligands, cytokine IFN-g) form classically activated macrophage (M1)
  2. Releases ROS, NO, lysosomal enzymes to destroy microbes
  3. Releases IL-1, IL-12, IL-23, chemokines to induce inflammation

Alternative:

  1. Monocyte (with cytokines IL-4 and IL-13) form alternatively activated macrophage (M2)
  2. Releases IL-10, TGF-B
  3. Aids tissue repair and termination of inflammation
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28
Q

Dendritic Cells

A

Antigen presenting cells

Produce cytokines to initiate inflammation and stimulate adaptive immune responses

Bridges innate and adaptive immunity

  1. Antigen captured by DC (immature)
  2. DC activated
  3. DC travels through lymphatic vessel to naive T cell
  4. Mature DC presents antigen to T cell

DC have lots of arms because its purpose is to tag onto things

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29
Q

Mast Cells

A

Abundant cytoplasmic and vasoactive granules
Skin and mucosal epithelium
More inflammatory than killing cell

  1. Activated by:
    >Microbial products binding to TLRs (innate immunity)
    >Antibody-dependent (allergic reactions)
  2. Vasoactive amines (histamines and tryptase)
    >Increase capillary permeability
    >Kill bacteria and inactivate microbial toxins
  3. Synthesize and secrete lipid mediators (prostaglandins) and cytokines (TNF)
    >Stimulate inflammation
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30
Q

Natural Killer (NK) Cells - CD16/56

A
  1. Identify infected and stressed cells and kill them
    >Empty cytoplasmic granules into extracellular space near the infected cell
    >Granules enter the cell and activate enzymes to induce apoptosis
  2. Intracellular microbial infections
    >Like tumors or viral infections
  3. Secrete IFN-g (macrophage activation)
  4. Activated by cytokines from macrophages and dendritic cells
    >IL-15: development and maturation of NK cells
    >IL-12 and type I IFNs: enhance NK cell killing function
31
Q

Activation of NK cells

A
  1. To eliminate cells infected with intracellular microbes
    >Antibody-dependent cellular cytotoxicity (ADCC)
    »CD16 cell surface marker specific for IgG bound to cells
    >Immunoreceptor tyrosine-based activation motifs (ITAMs) in their cytoplasmic tails
    »ITAMs become phosphorylated on tyrosine residues and recognize their activating ligands, promoting activation of cytosolic protein tyrosine kinases and activate other substrates involved in downstream signaling pathways causing cytotoxic granule exocytosis and production of IFN-g
  2. Eliminate injured cells and tumor cells with stress from DNA damage and malignant transformation
32
Q

Inhibition of NK cells

A

To block signaling by receptor activation specific for “self” MHC I molecules to protect healthy cells

Inhibitor receptors (on NK cell):
>Contain immunoreceptor tyrosine-based inhibitor motifs (ITIMs) that become phosphorylated on tyrosine residues when receptors bind to MHC I (on normal cell)
>Then bind and promote activation of cytosolic protein tyrosine phosphatases which remove the phosphate groups from the tyrosine residues of signaling molecules, counteracting ITAMs, blocking NK cell activation

Killer cell immunoglobulin-like receptors (KIRs)
CD94 and lectin subunit NKG2

33
Q

NK Cell ADCC

A

Antibody-dependent cellular cytotoxicity

Antibodies (IgG) recognize viral glycoproteins expressed on the surface of cells infected with the enveloped viruses

Therapeutic intervention in treating tumor cells

  1. IgG binds to surface antigens on antibody-coated cell
  2. Antibodies bind to CD16 on NK cell
  3. Killing of antibody-coated cell
34
Q

Complement System (Alternative, Classical, Lectin; C3a, C3b, C5a, C6-9)

A
  1. Initiation of complement activation:
    Alternative (innate)
    Triggered when activated complement proteins on microbial surfaces are uncontrolled due to lack of regulatory proteins

Classical (adaptive)
Triggered antibodies bound to microbes/antigens

Lectin (innate)
Mannose binding lectin (MBL) binds to terminal residues on microbial cell surface glycoproteins

All release complements that aid in next steps

  1. Early step:
    C3 > [help of complements from pathway] > C3b > C3a breaks off of C3b
    C3a: Inflammation
    C3b: OPSONIZATION and PHAGOCYTOSIS (C3b is deposited on microbe)

C5 > [help of C3b-microbe complex] > C5b > C5a breaks off of C5b
C5a: INFLAMMATION
C6-9: LYSIS of microbe (form membrane attack complex MAC)

35
Q

Membrane Attack Complex (Complement System)

A

C5 convertase causes proteolysis of C5 > C5b

C5b binds with C6, C7, C8, and C9s

Forms pore in cell membrane
Allows for influx of water and ions
Cell death

C6-9: Lysis of microbe

Activated by C3b

36
Q

Acute Phase Response

A

When plasma proteins increase rapidly with infection

37
Q

Collectins

A

Plasma proteins (innate)

  1. Mannose binding lectin (MBL):
    Recognizes microbial carbohydrates, coating them for phagocytosis
    Activation of complement by lectin pathway
  2. Surfactant:
    Soap like substance in the lung protective from infectious microbes
38
Q

C-reactive protein (CRP)

A

Plasma proteins (innate)

Binds phosphorylcholine on microbes, opsonizes them for phagocytosis by macrophages (CRP receptor)

Activates classical complement pathway proteins

Produced as part of the acute phase response and in the case of Gram+ bacteria, a common means of stimulation would be via TLR-2 on macrophages

39
Q

Cytokines (innate)

A

Interleukins

  1. Soluble proteins that cause cell signaling to generate immune and inflammatory reactions - stimulated by infection
  2. Communication between cells
  3. Produced by activated and act on leukocytes
  4. Innate immunity: mast cells, dendritic cells, macrophages
  5. Adaptive immunity: helper T lymphocytes
40
Q

TNFs, IL-1, Chemokines (cytokines)

A

Recruitment of neutrophils and monocytes

41
Q

TNF, IL-1 (cytokines)

A

Produce fever by acting on the hypothalamus

42
Q

IL-6 (cytokines)

A

Acute phase response protein synthesis from the liver: CRP and fibrinogen

43
Q

TNF at high concentration (cytokines)

A

Thrombus formation

Hypotension: reduced myocardial contractility and vascular dilation and leakage

44
Q

High TNF, IL-12 from dendritic cells and macrophages (in response to LPS and microbial molecules) - (cytokines)

A

Septic shock: hypotension, disseminated intravascular coagulation, metabolic disturbances

45
Q

Type 1 Interferon

A

Important in viral infections (creates antiviral state)

Type 1 interferon binds to the virus
>Blocking enzymes necessary for viral replication
>>Inhibiting protein synthesis
>>Degrading viral RNA
>>Inhibiting viral gene expression
46
Q

Tumor Necrosis Factor (TNF)

A

Cytokine

Cell source:
Macrophages, T cells, Mast cells

Cell target/bio effects:
Endothelial cells: activation (inflammation, coagulation)
Liver: synthesis of acute-phase proteins
Hypothalamus: fever
Neutrophils: activation
Muscle, fat: catabolism (cachexia)
Many cells: apoptosis

Increases the expression of MHCII molecules on APC

47
Q

Interleukin-1 (IL-1)

A

Cytokine

Cell source:
Macrophages, dendritic cells, endothelial, epithelial, mast cells

Cell target/bio effects:
Endothelial cells: activation
Hypothalamus: fever
Liver: synthesis of acute-phase proteins
T cells: Th17 differentiation
48
Q

Chemokines

A

Cytokine

Cell source:
Macrophages, endothelial cells, T cells, dendritic cells, fibroblasts, platelets

Cell target/bio effects:
Leukocytes: increase integrin affinity, chemotaxis, activation

49
Q

Interleukin-12 (IL-12)

A

Cytokine

Cell source:
Dendritic cells, macrophages

Cell target/bio effects:
NK cells and T cells: IFN-g production, increased cytotoxic activity
T cells: Th1 differentiation

50
Q

Interferon-g (IFN-g)

A

Cytokine

Cell source:
NK cells, T lymphocytes

Cell target/bio effects:
Activation of macrophages (Th1 response)
Stimulation of some antibody responses
Increased MHCI, MHCII expression

Only member of Type 2 IFN
Essential for Innate and adaptive immunity

51
Q

Type 1 IFNs (IFN-a, IFN-b)

A

Cytokine

Cell source:
IFN-a: Dendritic cells, macrophages
IFN-B: Fibroblasts
Leukocytes

Cell target/bio effects:
All cells: antiviral state, increased MHCI expression
NK cells: activation
Binds to INFAR1/INFAR2

IFNa only: increase MHCII expression

52
Q

Interleukin-10 (IL-10)

A

Cytokine

Cell source:
Macrophages, dendritic cells, T cells

Cell target/bio effects:
Macrophages, dendritic: inhibition of cytokine and chemokine production, REDUCED expression of costimulators and class II MHC

Calming effect
Reduces immune activation
(Can switch off T cells)

53
Q

Interleukin-6 (IL-6)

A

Cytokine

Cell source:
Macrophages (in response to PAMPs), endothelial cells, T cells

Cell target/bio effects:
Liver: synthesis of acute-phase proteins
B cells: proliferation of antibody producing cells

Mediator of fever

Crosses BBB and initiates synthesis of PGE2 in hypothalamus

54
Q

Interleukin-15 (IL-15)

A

Cytokine

Cell source:
Macrophages, others

Cell target/bio effects:
NK cells: proliferation
T cells: proliferation

55
Q

Interleukin-18 (IL-18)

A

Cytokine

Cell source:
Macrophages

Cell target/bio effects:
NK and T cells: IFN-g synthesis

56
Q

TGF-B

A

Cytokine

Cell source:
Many cells

Cell target/bio effects:
Inhibition of inflammation
T cells: differentiation of Th17, regulatory cells

Can switch off T cells

57
Q

Chronic granulomatous disease

A

Functional Deficiencies:
Defective production of reactive oxygen intermediates in phagocytes

Mechanisms of Defect:
Mutations in genes encoding phagocyte oxidase enzyme, mainly b558

58
Q

Leukocyte adhesion deficiency-1

A

Functional Deficiencies:
Absent or deficient expression of B2 integrins causing defective leukocyte adhesion-dependent functions

Mechanisms of Defect:
Mutations in gene encoding the B chain (CD18) of B2 integrins

59
Q

Leukocyte adhesion deficiency-2

A

Functional Deficiencies:
Absent or deficient expression of leukocyte ligands for E and P selectins, causing failure of leukocyte migration into the tissues

Mechanisms of Defect:
Mutation in the gene encoding a protein required for synthesis of the sialyl-Lewis X component of E and P selectin ligands

60
Q

Complement C3 Deficiency

A

Functional Deficiencies:
Defect in complement cascade activation

Mechanisms of Defect:
Mutation in the C3 gene

61
Q

Complement C2, C4 deficiency

A

Functional Deficiencies:
Deficient activation of classical pathway of complement leading to failure to clear immune complexes and development of lupus-like disease

Mechanisms of Defect:
Mutations in C2 or C4 gene

62
Q

Chediak-Higashi Syndrome

A

Functional Deficiencies:
Defective lysosomal function in neutrophils, macrophages, and dendritic cells, and defective granule function in natural killer cells

Mechanisms of Defect:
Mutation in a gene encoding a lysosomal trafficking regulatory protein

63
Q

Herpes Simplex Virus 1 (HSV-1) encephalitis

A

Functional Deficiencies:
Defective antiviral immunity in the CNS

Mechanisms of Defect:
Mutations in the TLR3 gene

64
Q

Recurrent pyogenic bacterial infections

A

Functional Deficiencies:
Defective innate immune response to pyogenic bacteria

Mechanisms of Defect:
Mutations in MyD88 gene

65
Q

Discrimination against self-antigens (Innate and Adaptive)

A

Prevent cell death and autoimmunity

Innate:
Receptors specific for PAMPs and DAMPs, not healthy substances
PRRs that recognize NAs (on normal cells) but located in cellular components where healthy cells are not accessible

Adaptive:
Lymphocytes that recognize self undergo apoptosis or are inactivated when they encounter self antigens

66
Q

IL-8

A

Chemotactic for neutrophils

67
Q

TNF-a

A

Improves cell surface molecules that improve adhesion of

Derived from monocytes and is a potent pyrogen

Causes fever directly or through IL-1; induces cachexia

68
Q

Superantigens (produced by, causes)

A

Exotoxins that cross-link TCR to Class II MHC

Instead of activating 1 in 10,000 T cells, as many as 1 in 5 are stimulated

Leads to massive IFN-g and IL-2 production

Acts on vascular endothelium to cause capillary leakage

Results in hypotension, shock, and death

Produced primarily by S. aureus and S. pyogenes

Causes:
Toxic shock syndrome

69
Q

S. aureus causes:

A
  1. Toxic shock syndrome

2. Sometimes food intoxication

70
Q

Treatment for TSS

A 
1. Manage infection
Blood culture
Antibiotics asap
Catheter replacement
Surgery?
2. Manage shock
Oxygen,  IV fluids
Breathing machines, kidney dialysis

Currently no drugs to target immune response

71
Q

Drugs under consideration for TSS

A
  1. Anti-inflammatory
  2. Drugs/immunotherapy targeting cytokines
  3. Anticoagulants
  4. Plasma exchange
  5. Vitamin/corticosteroids
    Vitamin C may improve blood flow to organs?
    Good results
  6. NSAIDS
    Help with blood flow
    Inhibit caspases
72
Q

Accelerate PhenoTest BC

A

Identification and antibiotic susceptibility of organisms for bloodstream infections

Identification in 90 min
Antibiotic susceptibility in 7 hours

73
Q

TSS

A

Sudden fever followed by headache, sore throat, diffuse red rash, skin desquamation

Shock within 48 hours

6,000/year

5/65% fatality with and without treatment

74
Q

TLR-4

A

Binds to LPS

Immunity (3 decks)

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