L16-17 Flashcards

(42 cards)

1
Q

Main defense against extracellular bacteria

A

opsonizing antibody and phagocytosis (esp for encapsulated bacteria), neutralizing antibody, complement

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2
Q

Encapsulated bacteria

A

hydrophilic capsule prevents phagocytosis unless opsonizing antibody + C3b are used to engulf bacteria

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3
Q

What complement molecule helps phagocytose encapsulated bacteria

A

C3b

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4
Q

neutropenic patients susceptible to

A

infections with extracellular pathogens

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5
Q

Splenectomized patients are susceptible to

A

sepsis (encapsulated bacteria)

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6
Q

Neutralizing antibody

A

inhibits attachment to receptors on host cells

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7
Q

Ig Deficiency patients are susceptible to

A

infections with extracellular pathogens

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8
Q

IgA defends

A

mucosal surfaces from infections

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9
Q

Anti-toxin antibodies

A

bind and neutralize toxin molecules by inhibiting them from binding to specific host cell receptors

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10
Q

endotoxins

A

LPS

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11
Q

Endotoxin is produced by

A

gram negative bacteria

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12
Q

Endotoxin structure

A

Lipid A core, highly variable carbohydrate side chains

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13
Q

Endotoxin vaccine?

A

no cannot be made into a toxoid due to stable Lipid A structure

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14
Q

Secondary immunity to endotoxin?

A

NO, highly variable structure will not recognized from another infection

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15
Q

Endotoxin triggers

A

alternative complement pathway

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16
Q

LPS is an exogenous pyrogen producing:

A

IL-1, TNF-alpha, IL-6

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17
Q

TLR4

A

PRR that binds CD14-LBP-LPS to induce macrophage response

18
Q

Exotoxin is produced by

A

gram negative bacteria or gram positive bacteria

19
Q

Exotoxin structure

A

distinct receptors, little variance, neutralizing antibodies are effective

20
Q

Tetanus

A

disease doesn’t always lead to immunity because toxins cause disease long before inducing an antibody response

21
Q

Exotoxin vaccine

22
Q

Superantigens

A

exotoxin capable of inducing large quantities of cytokines, by binding HLA class II molecules at non-binding site and activate all T cells with TCR allele

23
Q

Immunity to intracellular bacteria

A

CD4 producing IFN-gamma

24
Q

IFN-gamma

A

restricts protein synthesis by decreasing a.a. pool
decreased membrane fluidity to prevent entrance
NO production for bacterial toxicity
altered cell metabolism to inhibit bacterial growth
increased HLA Class I
activation of macrophages

25
Macrophage stimulation occurs by
IFN-gamma, LPS, TNF-alpha
26
Macrophage characteristics
increased vacuolization, increased respiratory burst, increased C3b and Fc receptors, increased HLA Class I and II expression, increased metabolism
27
CTL role in intracellular infection
delayed response after activation with IL-2, NK cells first responders
28
Obligate intracellular pathogens drive immune response towards
Th2 (antibody response) to slow Th1 response, they may also lay dormant until immune response wains
29
Humoral response to extracellular viral proteins
neutralizing antibody, opsonizing antibody (detrimental by providing entrance), classical complement pathway, or ADCC
30
Cellular immunity to intracellular viral proteins
NK cells (KIRS: lack of self HLA Class I), CTL, IFN-gamma
31
IFN-gamma's role in viral infection
restricts protein synthesis by decreasing a.a. pool decreased membrane fluidity to prevent entrance production of enzymes for destruction up regulation of HLA expression
32
Virus adaptation to evade immune response
``` block IFN activation pathway Block HLA molecule expression block complement activation Mutate themselves induce immune suppression ```
33
Protozoan parasite immunity
humoral protects from extracellular pathogens | CMI protects from intracellular pathogens
34
Parasitic helminths causes production of
IgE (allergy like symptoms) and eosinophilia
35
Parasitic helminths causes release of
IL-4, IL-5, and suppress IL-2 and IFN-gamma
36
Septic shock syndrome mediators
LPS, gram-positive peptidoglycan, f-met-leu-phe, 5'-mCPG, superantigens
37
Septic shock syndrome effects
circulatory collapse, DIC, hemorrhagic necrosis
38
By-stander immune pathology
damage to surrounding normal tissue
39
Autoimmunity
sharing of molecular structures may give way to cross-reactivity to host, Strep causing heart valve destruction called rheumatic fever
40
IgA, IgG, IgM
humoral response to virus, neutralization
41
IgG and IgM
humoral response to virus, opsonization
42
IFN-gamma
cellular response, induces anti-viral state