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Immuno Exam 2 > L16-17 > Flashcards

L16-17 Flashcards

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

A

yes, toxoid

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
Q

Macrophage stimulation occurs by

A

IFN-gamma, LPS, TNF-alpha

26
Q

Macrophage characteristics

A

increased vacuolization, increased respiratory burst, increased C3b and Fc receptors, increased HLA Class I and II expression, increased metabolism

27
Q

CTL role in intracellular infection

A

delayed response after activation with IL-2, NK cells first responders

28
Q

Obligate intracellular pathogens drive immune response towards

A

Th2 (antibody response) to slow Th1 response, they may also lay dormant until immune response wains

29
Q

Humoral response to extracellular viral proteins

A

neutralizing antibody, opsonizing antibody (detrimental by providing entrance), classical complement pathway, or ADCC

30
Q

Cellular immunity to intracellular viral proteins

A

NK cells (KIRS: lack of self HLA Class I), CTL, IFN-gamma

31
Q

IFN-gamma’s role in viral infection

A

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
Q

Virus adaptation to evade immune response

A 
block IFN activation pathway
Block HLA molecule expression
block complement activation
Mutate themselves
induce immune suppression
33
Q

Protozoan parasite immunity

A

humoral protects from extracellular pathogens

CMI protects from intracellular pathogens

34
Q

Parasitic helminths causes production of

A

IgE (allergy like symptoms) and eosinophilia

35
Q

Parasitic helminths causes release of

A

IL-4, IL-5, and suppress IL-2 and IFN-gamma

36
Q

Septic shock syndrome mediators

A

LPS, gram-positive peptidoglycan, f-met-leu-phe, 5’-mCPG, superantigens

37
Q

Septic shock syndrome effects

A

circulatory collapse, DIC, hemorrhagic necrosis

38
Q

By-stander immune pathology

A

damage to surrounding normal tissue

39
Q

Autoimmunity

A

sharing of molecular structures may give way to cross-reactivity to host, Strep causing heart valve destruction called rheumatic fever

40
Q

IgA, IgG, IgM

A

humoral response to virus, neutralization

41
Q

IgG and IgM

A

humoral response to virus, opsonization

42
Q

IFN-gamma

A

cellular response, induces anti-viral state

Immuno Exam 2 (6 decks)

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