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immunogenetics Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q

what does the disufide bond connect on an antibody

A

2 heavy chains

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2
Q

what part of the antibody activates complement and phagocytes

A

constant region

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3
Q

what part of the antibody binds to antigen

A

variable region

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4
Q

MCH is essential for…

A

antigen presentation to T cells

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5
Q

self MHC + foreign antigen=

A

T cell response

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6
Q

self MHC + self antigen=

A

no T cell response

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7
Q

no MCH + foreign antigen=

A

no t cell response

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8
Q

where is mhc located

A

every nucleated cell in the body

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9
Q

MHC 1 alters what

A

CD 8 + T cells because viruses infect these

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10
Q

____ is a key factor for determining tissue matching for transplant donors and recipients

A

MHC

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11
Q

MHC molecules have a broad specificity for peptides meaning….

A

many diff peptides can bind in the MHC binding cleft

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12
Q

true or false: peptides associated with mhc have a slow on and off rate

A

true

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13
Q

mhc haplotype of a person determines what

A

which peptides bind and how peptides bind

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14
Q

mhc genes are highly what

A

polymorphic

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15
Q

how many mhc alleles are in humans? how many recombinations?

A

hundreds of alleles with 10^13 recombinations

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16
Q

why is it hard to find transplant donors

A

mhc genes are highly polymorphic

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17
Q

how are mhc genes expressed?

A

condominantly meaning that all alleles are expressed at equal frequency

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18
Q

mhc haplotype?

A

set of mhc alleles on an individual chromosome

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19
Q

mhc haplotype can influence…

A

how an individual responds to certain pathogens
susceptibility to certain diseases
transplant success

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20
Q

first primary immunodeficiency disease to be descibed?

A

Bruton agammaglobulinemia

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21
Q

when are primary/congenital immunodeficiencies frequently manifested?

A

infancy and childhood

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22
Q

what are secondary/acquired immunodeficiencies a consequence of?

A

malnutrition, disseminated cancer, immunosuppressive drugs, infection of cells of the immune system

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23
Q

what is conserved across widely diverse species

A

TLR

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24
Q

what do primary immunodeficiency disorders affect

A

B cells, T cells, NK cells, phagocytic cells, and complement proteins

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25
Q

what may immunodeficiencies result from

A

defects in leukocyte maturation/activation or defects in effector mechanisms of innate and adaptive immunity

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26
Q

principle consequence of immunodeficiency?

A

inc susceptibility to infection

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27
Q

nature of infection in a pt depends on what

A

component of the immune system thats defective

28
Q

deficient humoral immunity results in inc susceptibility to fight infection by what

A

pyogenic bacteria

29
Q

what antibody isotopes are low in XLA/brutons agammaglobulinemia

A

ALL

30
Q

are circulating B cells present in XLA/brutons agammaglobulinemia

A

no

31
Q

are pre B cells present in XLA/brutons agammaglobulinemia

A

yes but they are reduced in number in the bone marrow

32
Q

tell me about the tonsil and lymph nodes in XLA/brutons agammaglobulinemia

A

tonsils are very small and lymph nodes are not palpable

33
Q

why are tonsils are very small and lymph nodes are not palpable in XLA/brutons agammaglobulinemia

A

absence of germinal centers

34
Q

tell me about the thymus in XLA/brutons agammaglobulinemia

A

theyre normal

35
Q

who is mainly affected with XLA/brutons agammaglobulinemia

A

boys

36
Q

why do boys not usually show symptoms of XLA/brutons agammaglobulinemia during the first 6-9 months of life

A

they still have the maternally transmitted IgG antibodies

37
Q

what happens after the maternal IgG antibodies wear off in XLA/brutons agammaglobulinemia

A

boys repeatedly get infections with extracellular pyogenic organisms such as pneumococci, streptococci, and haemophilus

38
Q

what type of defect is in XLA/brutons agammaglobulinemia

A

maturation of B cells

39
Q

in XLA/brutons agammaglobulinemia,
circulation B cells are____
pre B cells are_____

A

circulation B cells are absent

pre B cells are reduced

40
Q

what disease is associated with a loss of function of bruton tyrosine kinase

A

XLA/brutons agammaglobulinemia

41
Q

what is X linked immunodeficiency with hyper IgM characterized by

A

low serum IgG, IgA, IgE and increased IgM

42
Q

when do ppl with X linked immunodeficiency with hyper IgM usually become symptomatic

A

1st or 2nd year of life

43
Q

what types of infections do ppl with X linked immunodeficiency with hyper IgM or XLA have

A

pyogenic infections such as otitis media, sinusitis, pneumonia, tonsillitis

44
Q

what do pt with X linked immunodeficiency with hyper IgM that pt with XLA not have

A

hymphoid hyperplasia

45
Q

what is the defect in in X linked immunodeficiency with hyper IgM

A

loss of function of CD40 AKA CD154 ligand that’s expressed on helper T cells

46
Q

loss of CD40 or CD 154 prevents what

A

T cell from co-stimulating antigen specific B cells

47
Q

in this disease, B cells are not signaled by T cells to go through isotope switching and only make IgM

A

X linked immunodeficiency with hyper IgM

48
Q

trmt for humoral immunity deficiency

A

prophylactic antibiotics and/or gamma-globulin therapy

49
Q

2 diseases of humoral immunity?

A

X linked immunodeficiency with hyper IgM and XLA/brutons

50
Q

deficient cell mediated immunity results in inc susceptibility to fight infection by what

A

viruses and other intracellular pathogens

51
Q

trmt for deficient T cell responses?

A

there arent really any (BMT and gene therapy for now); pts usually only live til infancy or childhood

52
Q

what does not develop in DiGeorge syndrome

A

thymus and therefore T cells

53
Q

what causes thymic hypoplasia in DiGeorge synd

A

defects in morphogenesis in 3rd and 4th pharyngeal pouches during early embryogenesis

54
Q

what happens with B and T cells in DiGeorge synd

A

T cells decreased and B cells increased

55
Q

how do most infants with DiGeorge synd die in first few months/years of life

A

infections, CV defects, seizures

56
Q

where are clinical similarities btwn DiGeorge synd and what other synd

A

fetal alcohol

57
Q

what is there a deficiency in in XLR SCID?

A

T and B cell function; they have few or no T cells and NK cells, but increased B cells

58
Q

mc form of SCID

A

X liked SCID/XSCID

59
Q

what do infants with XSCID present with in 1st few months of life

A

diarrhea, pneumonia, otitis, sepsis, cutaneous infections

60
Q

candida albicans, pneumocystis carinii, varicella, measles, parainfluenzae, cytomegalovirus, and EBV are in what disease

A

XLR SCID

61
Q

what do pts with XLR SCID lack

A

ability to reject foreign tissue so theyre at greater risk for GVHD

62
Q

what can GVHD result from

A

maternal T cells that cross into the fetal circulation while the SCID infant is in utero

63
Q

what is wrong with B cells in XLR SCID

A

they dont produce Ig normally

64
Q

what are the 2 aims of current trmts of immunodeficienceis

A

minimize and control infection and replace defective/absent components

65
Q

trmt of choice for immunodeficiencies rn?

A

BMT

Medical Genetics (15 decks)

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