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Immunology > Immunology MCM Unit 1 > Flashcards

Immunology MCM Unit 1 Flashcards

1
Q

opsonin

A

something that increases the phagocytosis of an object by binding to it
-CD3 is a opsonin for many effector cell types

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2
Q

complement

A

group of serum proteins involved in innate and adaptive response. important for inflammation and removing bacteria. bind to microbes firectly or to antibodies. often lyses target.

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3
Q

CD Antigens

A 
cluster of differentiation. for cell surface antigens on leukocytes to differentiate lineage/maturation state 
for T cells:
CD3 - Mature T cells
CD4 - helper T
CD8 - cytotoxic T cells
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4
Q

primary lymphoid organs

A

where immune cells are made. include bone marrow and thymus (site of T cell maturation)

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5
Q

secondary lymphoid organs

A

where immune cells do the work. includes lymphnodes (filter, make Abs, trap pathogens, exchange with blood), mucous membranes, spleen (macrophages and T cells here, removes RBCs and platelets)

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6
Q

how to define immune cells

A

morphologically - acid/base stain, size and shape of cell and nuleus

antigenic - monoclonal antibodies can recognize T cells, Bcells, and subtypes of T cells. use CD cluster of Differentiation notation to separate based on reactivity group. Common ones are CD3, CD4, CD8.

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7
Q

neutrophil/PMN

A
  • most abundant leukocyte (60%)
  • get to site of inflammation first
  • engulf by phagocytosis then kill with granules full of hydrolytic and bactericidal enzymes. then they die
  • only circulate for 12 hrs
  • end myeloid cells; do not differentiate
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8
Q

eosinophils

A
  • 1-3% of WBC
  • short 1/2 life of 30 min
  • releases granules full of Eosinophilic basic protein (EBP) to clear parasitic worms
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9
Q

basophil

A

stain basic

control parasites with unknown mechanism

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10
Q

macrophage

A
  • phagocytosis and killing
  • intracellular killing of bacteria, yeast and parasites
  • extracellular kill of virally infected cells, large parasites and tumor cells
  • APC are macrophaes
  • activate T cells and initiate immune response
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11
Q

monocytes

A

precursor to macrophages

  • derived in bone marrow and circulate in blood
  • when they enter tissue they become macrophages
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12
Q

mast cell

A

get rid of parasites by releasing granules full of histamine and others. important in innate immunity and allergies

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13
Q

dendritic cell

A

activate T cells and initiate adaptive response

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14
Q

B cells

A
  • has immunoglobulin on surface
  • makes Antibodies
  • activated by T helpers. divide into plasma and memory cells
  • plasma produce Ab that flood blood stream, bind atigens and mark for destruction
  • memory cells last forever and make 2nd response. these B cells already did class switch to igG so quicker
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15
Q

T cells

A

regulate immune response and kill infected cells

-T helper cells recognize specific antigens

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16
Q

Cytotoxic T cells

A

regulation and effector cells
have CD8
kill cells with self plus foreign antigen - only a limited number of targets (infected and tumor cells)
-binds and kill with enzymes

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17
Q

Natural Killer cells

A
  • large granular lymphocytes
  • kills tumor and virally infected cells without specificity
  • part of innate immunity. similar function to Tc cells
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18
Q

lymphoid cells

A

B, T, NKs

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19
Q

cytokines

A

general term. alter response of immune system

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20
Q

igM

A

predominates in premature immune response

  • agglutinating + antigen receptor on B cells
  • opsonizing and bacteriolytic w help of complement
  • 4 heavy chain domains andJ chain
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21
Q

IgG

A
  • predominate in serum
  • agglutinizing, opsonizing, neutralizing, bacteriolytic
  • subclasses 1,2,3,4
  • intrachain disulfide bonds
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22
Q

IgA

A
  • predominates in secretions
  • opsonizing and agglutinating
  • T piece resists acid hydrolysis
  • J chain
  • monomer, dimer or trimer
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23
Q

IgE

A
  • hypersensitivity/allergies
  • binds to mast cells
  • regulates vascular elasticity
  • defends against parasites
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24
Q

primary immune response

A
  • long lag phase
  • log/exponential growth
  • goes away quickly
  • primarily IgM then IgG
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25
Q

secondary immune response

A
  • shorter lag phase
  • higher rate of antibody synthesis
  • longer persistence
  • predominately IgG
  • antibodies with higher affinity
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26
Q

toxin vs toxoid

A

toxin made by anything living. toxoid is non-toxic but will still stimulate immune response

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27
Q

Antigen presenting cells

A
  • initiate interaction with antigen by endocytosis
  • may be enhanced by complement/pre-existing Ab or specific receptors for the pathogen
  • degrade and then deposit antigen on the surface
  • requires a co-stimulatory signal; commonly B7
  • T helper cells recognize specific antigens on surface
  • IL1 released by APC, stimulates T helpers to release IL2, causes proliferation of Tc and B cels
28
Q

mendelian disease

A

mutation in one gene causes disease

29
Q

multifactorial disease

A

need mutation in several genes at one time to cause disease

30
Q

autosomal dominant

A

one mutated is enough to cause disease

  • most effected are heterozygous
  • in every generation
  • affected people have affected parents
  • normal people dont have affected offspring
  • both sexes
  • vertical pattern
  • reoccurence is 50%
  • male –> male means not x-linked
  • ex: Huntingtons disease
31
Q

Autosomal recessive

A
  • both parents of affected individual are carriers
  • parents usually asymptomatic
  • horizontal pattern
  • both sexes
  • recurrence risk 25%
  • offspring carrier risk is 50% before birth, increases to 2/3 if they are born unaffected
  • 1 grandparent is a carrier, each has 50% chance
  • related aunt/uncles has 50% chance of being carrier and cousin 25% chance
  • ex: Cystic Fibrosis
32
Q

x-linked dominant

A
  • affected males have normal sons and affected daughters
  • 2x as many females as males
  • most affected females are heterozygous so 1/2 their offspring are affected
  • more severe in men
33
Q

mitochondrial inheritance

A

inherited through females only

  • all offspring of an affected female is affected
  • affected males will not pass it on
  • highly mutatable
  • variable expression and lack of penetrance
34
Q

new germline mutation

A

permanent change to DNA that can be inherited through gamete

35
Q

chimerism

A

derived from cells from 2 zygotes

-transplant or DNA from unborn fraternal twin

36
Q

mosaic

A

tissue has 2+ cell lines but from one zygote

  • looks patchy
  • leukemia
37
Q

expressitivity

A

mild vs. severe

  • phenotype depends on severity of mutation
  • mild mutation in CFTR gene will hurt the vas deferens but it takes a severe mutation in CFTR gene to effect the pancreas
38
Q

penetrance

A

presence or absence of phenotype effect

39
Q

locus vs allelic vs clincal/phenotypic hetergenity

A

locus - same phenotype/disease from mutation in different gene
allelic heterogenity - different mutation on same gene
clinical/phenotypic - variation in phenotype/disease from a mutation in one gene because difference in expressivity or penetrence

40
Q

innate vs. immune

A

innate: non-specific, quick, skin and stomach, uses complement system
adaptive: specific, longer lasting, 2nd to respond, involves B and T cells

41
Q

antibodies

A

serum proteins

  • specific immune response
  • bind specifically to antigens at N terminus
  • Fc region binds effector cells + proteins
42
Q

classes of antibodies

A 
G, M, D, A, E
all Ig classes have different heavy chains
all have diff molecular mass
IgG most abundant and lasts longest
IgE least abundant and shortest 1/2 life
43
Q

Functions of antibodies

A
  1. neutralize - G, A
  2. IgG 1 &3
  3. Sensitization for killingby NK - IgG
  4. Sensitization of mast cells - E
  5. basophils - D and E
  6. activate complement - M&G
  7. transport across epithelium - A
  8. across placenta - G
  9. diffuse across extravascular sites - G&A
44
Q

proteins present in immunoglobulins

A

albumin and several globulins

45
Q

complement system

A

uses cascade signaling through 3 possible pathways

  1. classical - Ab binds antigen. complement binds Fc and cleaves - 1 subunit of each C 1,2,3 binds antigen and other subunit released
  2. Alternative - bind foreign substance without Ab
46
Q

clonal selection theory

A

antibodies with highest affinity are selected for over time

47
Q

Hapten

A

cannot make Ab to it. need a carrier protein for T helper to recognize

48
Q

how antibodies bind antigens

A

variable regions have framework regions that are similar amongst antibodies and help fold regions

  • hypervariable regions have specific AAs thatcode for specific antigen binding site
  • 3 hypervariable regions per heavy and light chain each
49
Q

multivalent antibodies

A
  • can bind two antigens with similar structure
  • a single antigen will produce several different antibodies for different epitopes with different affinities
  • purify with adsorption or affinity chromatography
50
Q

how to make monoclonal antibody

A

monoclonal comes from 1 antibody so they are identical

  • less avidity
  • make good drugs
  • started with mice, but mice antibodies are antigen in human
    1. inject mouse with antigen
    2. isolate spleen cells where B cells made
    3. fuse it to tumor cells that can grow forever
    4. grow hybrids in selective media
    5. clone hybrids so cells grow independently
    6. select individual clone with specificity you’re interested in
51
Q

cross reactivity

A

antiserum binds to other antigens besides the specific antigen you want

52
Q

avidity

A

strength of binding of multivalent antiserum to multivalent antigen

53
Q

4 types of monoclonal antibody developed

A
  1. mouse (-omab)
  2. chimeric - mouse variable on human constant (-ximab)
  3. humanized - mouse hypervariable on human (-zumab)
  4. human -no mouse. made through biotechnology (-umab)
54
Q

ELISA

A
  • antigen stuck to well
  • add antibody,then wash unbound
  • add 2nd antibody with enzyme which sticks to 1st Ab, then wash unbound
  • add chemical that turns color if enzyme bound is present
  • used for Ab or antigen assay
55
Q

immunofluorescence

A
  • add antisera for specific pathogen/cell marker
  • add 2nd Ab that binds 1st Ab and has fluorescent mlc attached
  • view under UV light. fluorescently bound molecules emit visible light
  • can be used to identify cell structure or pathogen in a cell
56
Q

immunohistochemistry

A

stain 1st and 2nd antibody with attached enzyme (peroxidase)

-chemicals that react with peroxidase stain tissue brown or red

57
Q

flow cytometry

A
  • immunofluorescence automated
  • pass cells through detector with lasers
  • tell amount of antibodies (++, +-, –)
  • may sort too.
58
Q

western blot

A
  • use SDS and separate proteins based on size
  • place separate proteins on nitrocellulose paper
  • add antibodies, specific antiserum binds, wash away unbound
  • detect antibody with enzyme linked IgG
  • can determine amount, molecular weight and type of antigen
59
Q

how V, D and J regions brought together during gene rearrangement in B cells

A

RAG enzymes.
First bring D and J together - get rid of RSSs hepatmer signal sequence and do hair pin flip to create palindromic P region.
-tDT adds random nucleotides
-repair enzymes pair nucleotides and exonucleases excise ones that dont pair
-often the reading frame is shifted and the B/T cell will not develop

-to join V to DJ regions, Rag makes a loop of regions to be cut out

60
Q

ways to get immunological gene arrangement diveristy

A
  1. recombination
  2. junctional diversity
  3. somatic hypermutation
61
Q

order of immunological rearrangement

A
  1. D and J regions both chromosomes
  2. V to DJ on one chromosome (2nd chromosome if it doesnt work)
  3. rearrange kappa on 1 chromosome (then other kappa then the lambdas if the others dont work)
    - wind up with unique antigen binding site
62
Q

switch from IgM to IgD

A 
splicing of RNA transcript. doesnt do class switch. this is not a permanent change because new RNA always being made. 
-RNA splicing is also how secreted vs. membrane IgG is determined
63
Q

how class switching works

A

when antigen binds and B cell needs to mature, there is class switch from IgM to IgG

  • AID enzyme recognizes switch signals in between constant regions and cuts DNA
  • cut out constant regions you dont want like IgM and IgD (in a loop that gets cut out) and put the variable region next to new constant region you want
  • a permanent change because you splice out DNA
64
Q

somatic hypermutation

A

during class switch, there is a high mutation rate in the V and J regions. mutations that increase binding affinity will be selected for.

65
Q

how B and T cell mechanism of formation differs

A

same except that T cells do not have somatic hypermutation

Immunology (3 decks)

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