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HDID 1 > 2. Innate Immunity and Inflamm I > Flashcards

2. Innate Immunity and Inflamm I Flashcards

1
Q

the inability to mount a response to infection is often _____.

A

lethal

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2
Q

the innate immune response is most closely associated with ________, the adaptive immune response is secondary to the innate immune response and is ______.

A

inflammation (generate cytokines, inflammatory signals), antigen-specific (humoral = antibody, cell-mediated = CMI)

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3
Q

define immunology

A

the study of all aspects of host defense against infection and of adverse consequences of the immune system

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4
Q

is innate or adaptive immunity evolutionary older?

A

innate

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5
Q

the innate immune response uses _____ to be activated.

A

pattern recognition of microbial products

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6
Q

how does the innate immune response initiate adaptive immune responses?

A

up-regulating co-stimulatory molecs on APCs and by producing cytokines

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7
Q

the adaptive immune response requires ____ recognition

A

epitope (to generate production of Abs or cytotoxic T cells)

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8
Q

which is stronger, innate or adaptive immunity?

A

adaptive

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9
Q

adaptive immunity involves _____ expansion of antigen-specific cells

A

clonal

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10
Q

receptors of innate immunity vs receptors of adaptive immunity

A

innate: encoded in germline; limited diversity (pattern recognition receptors) (eg TLR, N-formyl peptide receptor, mannose receptor, or scavenger receptor)
adaptive: encoded by genes produced by somatic recombination of gene segments; greater diversity

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11
Q

receptor distribution, innate vs adaptive

A

innate: nonclonal (identical receptors on all cells o the same lineage)
adaptive: clones of lymphocytes with distinct specificities express different receptors

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12
Q

discrimination of self and nonself in innate immunity

A

healthy host cells are not recofnized or they may express molecs that prevent innate immune reactions (but some host molecs trigger the innate immune response: eg uric acid leading to inflammation = gout)

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13
Q

discrimination of self and nonself in adaptive immunity

A

based on selection against self-reactive lymphocytes (may be imperfect, giving rise to autoimmunity)

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14
Q

three important functions of innate immunity

A
  1. prevents infection of host (can elim microbes) - lack of innate immunity increases susceptibility to infection
    • earliest sensor of danger to the host
  2. effector mechanisms used in innate immunity - used to eliminate microbes, even in the adaptive response (cytokines produced as a conseq of adaptive immunity, like IFN-gamma, can act on macrophages to cause them to become more microbicidal)
  3. stimulates adaptive responses; influences nature of adaptive response (tailors adaptive response to different microbes, eg IL-4 facors the development of a humoral Th2 Ab response)
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15
Q

a defect in innate immunity lets the organism replicate early in infection - there is no control of what?

A

no ability to control microbial replication

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16
Q

a defect in adaptive immunity, the replication of the pathogen is controlled early in infection, but what happens?

A

failure to clear the infection

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17
Q

mechanical, chemical, and microbial mechanisms are all part of the ____ defenses of the innate immune system.

A

external

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18
Q

complement, phagocytic cells and non-phagocytic cells are all part of the _____ defenses of the innate immune system.

A

internal

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19
Q

______ represent a continuum that protects the host from infection - very large surface area represented by these.

A

skin and mucus membranes

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20
Q

what is the most important non-specific means of preventing infection?

A

skin (so real problem for burn patients)

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21
Q

what are the 4 aspects of how skin acts as part of the external defense system?

A
  1. keratinized outer layers (rarely penetrated)
  2. cellular contiguity (tight junctions)
  3. dring (desiccation) and sloughing of bacteria on skin surface
  4. sweat glands - unsaturated fatty acids are ANTIBACTERIAL
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22
Q

injury to mucus membranes often leads to invasion by what?

A

normal flora (big problem re: surgery)

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23
Q

what does mucus do re: external defense?

A

holds bacteria away from cell surface and traps bacteria

24
Q

what do cilia do re: external defense?

A

sweeps mucus away (eg up towards throat to be swallowed and thus bacteria destroyed)

problem for smokers with damaged cilia and CF patients with too much mucus

25
Q

what are the 4 ways in which the GU tract participates in external defense?

A
  1. washing of urine
  2. acidity of urine
  3. lysozyme
  4. vaginal lactic acid (controls fungi)
26
Q

how do eyes participate in external defense?

A
  1. lavaging action re: tears

2. lysozyme in tears cleaves the bond b/w bacterial cell wall components (eg N-acetylglucosamine and muramic acid)

27
Q

how does the GI tract flora participate in external defense

A

normally, symbiotic with host. Produce bacteriocins that kill other pathogens; compete with more pathogenic microbes for nutrients

28
Q

in the GU tract, exfolaition of epithelial cells inhibits microbial colonization of the mucosa - how do microbes take advantage of this?

A

pathogens suppress this host defense by upregulating expression of adhesion molecs that prevent cells from exfoliating

29
Q

host-derived antimicrobial peptides, general facts:
chemical structure?
activity?
found where?

A

short, cationic, broad-spectrum antimicrobial proteins

membranolytic activity

found in myeloid cells (neutrophils/alveolar macrophages)

found at mucosal surfaces (trachea, small intestine, female reproductive tract)

30
Q

because lots of pathogens need Fe++ to survive, how does our innate immune system handle this?

A

transferrin and lactoferrin are iron-binding proteins that compete with bacteria for iron

31
Q

what are defensins?

A

basic, CYSTEINE-rich antimicrobial peptides (subclass of anti-microbial peptides)

found in PMN, macrophages, paneth cells in crypts

broad spectrum antibiotic: gram +/- bacteria, fungi, enveloped virus, and mycobacterium (just have to be in the right place at the right time)

sequential permeabilization of outer and inner bacterial membranes to form membrane channels and kill things

some defensins are also chemotactic (attract white cells to site of production)

32
Q

interferons (IFNs) - generally what are they?

A

antiviral cytokines w/ macrophage activating activity

33
Q

Type I IFNs (IFN-alpha/beta) - what do they do?

A
  1. induce resistance to virus infection in all cells (protects uninfected cells and produced by virus-infected cells)
  2. increase MHC I expression and antigen presentation to CD8+ T cells, activates macrophages to make them more phagocytic and microbicidal
  3. activates NK cells to kill virus-infected cells
34
Q

series of enzymes in serum/tissues that participates in innate immune response by increasing vascular permeability, acting as a chemotactic factor, and coating (opsonizing) bacteria to increase their uptake by phagocytes; complement byproducts have phlogistic activities: increase vascular permeability and cell adhesion molecules….what is this describing?

A

complement

35
Q

in the classical activation of complement, antibody binds to surface of microbe (or host cell) and then the Ab binds complement through its _______, leading to complement activation.

A

Fc portion

36
Q

microbial antagonism - three main aspects of innate immunity external defense

A

Normal flora (commensal); “microbiota” – symbiotic relationship with host

	a. compete for nutrients required for pathogenic organisms
	b. release of “bacteriocins” (e.g., E. coli inhibition of Salmonella)
	c. “tonic” stimulation leads to low level of inflammation (this helps to facilitate control of more pathogenic organisms)
37
Q

what are the anatomic barriers involved in the internal defense of the innate immune system?

A

fibrous capsules around internal organs

38
Q

what does PMN stand for?

A

polymorphonucleated neutrophil (enzyme filled granules kill/digest bacteria)

39
Q

what ar ehte major cell types of the innate immune defense internal mechanisms?

A

PMNs (neutrophils), mononuclear phagocytes (monocytes/macrophages), NK cells

40
Q

what are macrophages of the kidney called?

A

glomerular mesangial cells

41
Q

what are macrophages of teh CT called?

A

CT histiocytes

42
Q

what is the main function of kupffer cells?

A

detox

43
Q

circulating monocytes vs resident macrophages?

A 
circulating monocytes:
home to inflamed tissues
- kill pathogens
- presentation of antigens
- activate other immune cells
resident macrophages:
found throughout the body
- removal of debris
- aid in tissue remodeling
- inhibit immune responses
44
Q

when are PMNs mature?

A

when they enter circulation

45
Q

monocytes and PMNs come from a common stem cell - what drive lineage pathwya?

A

colony stimulating factors (they’re cytokines) (G-CSF= granulocyte CSF to PMN; M-CSF = monocyte CSF - CSF-1 for monocytes)…occurs in the bone marrow

46
Q

longevity of PMNs vs macrophages?

A

PMNs - short (hours to days)

macrophages - long (years)

47
Q

relative numbers of PMNs vs macrophages?

A

PMNs: 30-70% circulating white blood cells, half that number are adherent to vessel walls (margining PMNs); 100X in bone marrow pool

monocytes: 3-7% of circulating white blood cells, large, fixed differentiated pops in tissues

48
Q

4 steps of leukocyte trafficking

A
  1. tethering (selectins, goes from 4000 to 40 mm/sec)
  2. activation (chemokines, 1-20 sec)
  3. adhesion/arrest (integrin/CAM)
  4. transendothelial migration (10 min) (diapedesis)
49
Q

characteristsics of chemokine receptors on phagocytes?

A

7 TM, GPCR, rapidly activate changes in actin polymerization leading to cytoskeletal rearrangement and mvmt

50
Q

which extravasate first - neutrophils or monocytes?

A

neutrophils (they are more numerous)

51
Q

arrival of neutrophils/macrophages at tissue infection site?

A

When the neutrophils arrive at the tissue site, they degranulate (release of granules that contain many enzymes and other proteins that are microbicidal); they die rapidly. The monocytes then come in secondarily to clean up the site of infection. Macrophage activation is very dependent upon coordinate signaling through various receptors on the cells.

52
Q

macrophage activation is driven by encironmental stimuli (bacterial products and cytokines) - classical activation?

A

in response to strong bacterial stimulus (eg LPS) and proinflammatory cytokines (eg IFN-gamma), highly microbicidal/tumoricidal cells; can cause inflammatory damage to surrounding tissues - strong producers of TNF-alpha, IL-1Beta, and other proinflammatory cytokines

generally induced by potent inflammatory cytokines (e.g., IFN-gamma) and TLR agonists (e.g., LPS). Leads to production of proinflammatory gene products (e.g., cytokines like TNFalpha, IL-1beta); increases enzymes that drive production of nitric oxide or reactive oxygen intermediates (see below). While such macrophages are strongly microbicidal, release of such products can cause tissue damage.

53
Q

macrophage activation is driven by encironmental stimuli (bacterial products and cytokines) - alternative activation?

A

induced by IL-4 or IL-13, increases mannose receptors, enzymes that contribute to wound/tissue repair (eg FIZZ1, Ym1); anti-inflammatory cytokines (eg IL-10); associated primarily with parasitic infections and allergy

Certain cytokines produced by Th2 cells or by infected macrophages (e.g. IL-4 or IL-13), drive differentiation to produce a distinct set of enzymes and cytokines (see fig). These macrophages are mostly involved in wound repair and tissue remodeling; however, recent studies have shown that certain pathogens drive this kind of differentiation to permit intracellular replication.

54
Q

macrophage differentiation is referred to as ____ becaus ethey can de-differentiate and re-differentiate

A

plastic

55
Q

alarmins, chemokines, lipid mediators, or N-formylmethionyl peptides binding to 7 TM receptors leads to what?

A

increased integrin avidity; cytoskeletal changes

and migration into tissues

56
Q

microbes binding to TLRs leads to what?

A

produciton of cytokines, reactive oxygen intermediate (ROIs)

and killing of microbes

57
Q

mannose binding the mannose receptor leads to what?

A

phagocytosis of microbe into phagosome

and killing of microbes

HDID 1 (24 decks)

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