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Module 5 Hematology > Immunoglobulins > Flashcards

Immunoglobulins Flashcards

1
Q

what is innate immunity

A

defends against nospecific manner

Phagocytes, Neutrophils, Natural Killer Cells (NKC)

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2
Q

5 types of innate immunity

A 
mechanical 
chemical 
micorbial 
complement system 
toll like receptors
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3
Q

mechanical barries

innate immunity

A

skin
hair
mucus
macrophages

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4
Q

chemical barriers

A

hyrdolytic enzyme of saliva
stomach acid
proteolytic enzymes of bile
low ph in the vagina

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5
Q

properties of innate immune system

A

characteristics

immune components

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6
Q

characteristics of immune system

A

Antigen Nonspecific: attacks foreign bodies
› Rapid response (Mins to Hrs)
› No memory

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7
Q

properties of immune system

A 
IMMUNE COMPONENTS
› Natural barriers
› Phagocytes and NK cells
› Soluble mediators
› Pattern recognition molecule
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8
Q

cells in the innate immune system

A 
polumorphnuclear cells 
Macrophages 
dendritic cells 
natural killer cells 
innate lymphoid cells
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9
Q

cell in the innate system
- has basophils, neutrophils, eosinophils.
produces - peroxide, superoxide radicals, nitric oxide

short lived in phagocytic

A

Polymorphnuclear cells

PMN’s

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10
Q

cell in the innate system

  • phagocytes derived from blood monocytes
  • small sperical cell
  • little er
  • abundant cytoplasm
A

Macrophages

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11
Q

Migration of different macrophages

Kupffer cells 
Alveolar 
Splenic 
Peritoneal macrophages 
Microglial
A

Kupffer cells - liver

  • Alveolar macrophages - lungs
  • Splenic macrophages - spleen (red pulp)
  • Peritoneal macrophage - peritoneal fluid
  • Microglial cells - CNS
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12
Q

cell in the innate system

  • efficient APC that enables them to trigger adaptotive immune response by T cells
  • plasmatocytoid
A

Dendritic cells

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13
Q

this is another type of dendritic cells

  • derived from lymphoid precursor cell
  • ability to produce large amounts of beta/alpha interferos in response to viral bacterial stimuli
A

Plasmatocytoid dendritic cells

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14
Q

cell in the innate system
- can recognize abnormal cells usch as cancer cells
- plays role in early stages of viral infection or
tumorogenesis before the large number of activated
cytotoxic T lymphocytes are generated
- large granular lymphocyte leading to LYSIS

A

Natural killer cells

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15
Q

the process of disintegrating cells

A

Lysis

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16
Q

these are the receptors in NKC

A

KILLER CELL
INHIBITORY RECEPTOR which binds to MHC-1
expressed in normal cells

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17
Q

what happens to virus infected cells

A

Virus infected cells and tumor cells have
significantly reduced MHC-1 molecules on their
surface and the killer cell inhibitory receptor

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18
Q

when NKC fails to engage to MHC-1

A

will fail to engage to the MHC-1 therefore

becoming susceptible to NK cell mediated toxicity

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19
Q

cell in the innate system

  • heterogeneous family
  • associated with airway and gut inflammation
  • diverse in making cytokines
A

INNATE LYMPHOID CELLS

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20
Q

this system

  • plays a major role in defense against infections
  • both innate and adaptive immune
  • enhances pathways that remove pathogens
A

COMPLEMENT SYSTEM

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21
Q

The Three Complement Pathway

A

-CLASSICAL PATHWAY
-LECTIN PATHWAY
- ALTERNATIVE
PATHWAY

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22
Q

this complement system pathway

- when c1 binds to antigen antibody to comples

A

Classical pathway

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23
Q

this complement system pathway

  • when MBL binds to terminal polysaccharide residue on surface
  • activated protein called Ficolin binds to acetylated microbial surface
A

Lectin Pathway

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24
Q

this complement system pathway

- when C3B deposit on surface of the pathogen

A

Alternate pathway

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25
Q

contributes to immunity and protection againts foreign objects

A

Immunoglobulins

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26
Q

immunoglobulins have 5 heavy chains with each have unique properties

A 
G
A
M
E
D
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27
Q

what are the 5 heavy chains used to catergorize antibodies as

A

Isotypes

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28
Q

when there are minor differences in the major strains

occuring between individuals

A

Aliotypes

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29
Q

monomeric in cell surface but secreted by

plasma cell as pentamers

A

IgM

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30
Q

monomeric in cell surface and is secreted a

monomer or as a dimer

A

IgG

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31
Q

– not secreted

A

IgD

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32
Q

secreted as monomers

A

IgE and IgA

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33
Q

this immuno globulin

  • earliest synthesized- Fetus
  • 20WOG maternal
  • short lived
  • primary response of antigen
  • does not deffuse well
  • 5-10%
A

Immunoglobulin M

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34
Q

presence of this immunoglobulin shows intrauterine infection

Monomeric IgM is the major antibody receptor on the
surface of B lymphocytes for antigen recognition. remains largely confined to bloodstream (80%).

A

Immuniglobulin M

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35
Q

helps detect congenital infections such as

toxoplasmosis, syphilis, rubella, cytomegalovirus infection and HIV infection.

A

Immuno M

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36
Q

highest avidity of all immunoglobulins for antigens with multiple epitopes

  • better agglutinin than other antibody isotypes.
A

Immuniglobulin M

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37
Q

more efficient than IgG

takes less than 100 to 1000 times than

less is required to neutralize viral interactivity

A

Immuniglobulin M

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38
Q

what happens when there is deficiency of LgM

A

Septicemias

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39
Q

what is the function of LGM

A

primary response to antigen

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40
Q

what does lgm promote

A

phagocytosis

potent activators of complement

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41
Q

properties of lgm and location

A

3rd Most common serum (5-10%)
› Half-life in serum: 5 days
› Cannot cross placenta

Blood- Lymph- B cell surface

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42
Q
  • Major immunoglobulin 85%
  • 2 heavy chains and 2 light chains
  • divalent
  • 15% of healthy proteins in humans
  • all 4 chains differ in loc and chains
  • 75% antibodies of the body
A

LgG

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43
Q

in terms of complement activation power

A

IgG1 and IgG3 fix C1q = most effectively

IgG2 = weakly

IgG4 = does NOT bind complement…

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44
Q

what is the life of Lgg

A

IgG3: 7 to 8 days

IgG1, IgG2, and IgG4: approximately 21 to
24 days

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45
Q

key player in humoral immnue response
- reacts to MacroP, Neutrophils, NKCs

  • y heavy chain
A

Lgg

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46
Q

location of Lgg

A

Location: blood, lymph fluid, cerebrospinal fluid

and peritoneal fluids.

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47
Q

diseases when an increase in lgg occurs

A

-Hyperimmunization
-Chronic Granulomatous
Infection
-Malnutrition
-Liver Disease

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48
Q

diseases when an decreases in lgg occurs

A
  • Lymphoid Aplasia
  • CLL
  • Selective IgG and IgA
    Deficiency
  • Agammaglobulinemia
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49
Q

what are the lgg subclasses and %

A

Lgg1 60-70%
Lgg2 - 20-30%
Lgg3 - 5-8%
Lgg 4 1-4%

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50
Q
  • most abundant type of lgg class
  • responsible for thymus mediated immune response
  • can cross placenta
A

Lgg1

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51
Q

this lgg class activates classical pathway of the complement cascade via C1 complex

A

Lgg1

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52
Q

this type of lgg class

  • shorter hinges
  • poor activators
  • only 1 alloted
  • less susceptible to cleavage by proteoglycans
A

Lgg2

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53
Q

function of this lgg class is to almost exclusive anti-polysaccharide response

  • in host defense against encapsulated bacteria
  • activates both classical and alternative cs
  • induces opsonization
A

lgg2

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54
Q

an immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes.

A

opsonization

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55
Q 
this type of lgg
- extended hinges
- greater flexibility 
- susceptible to proteolyytic enzymes like pepsin, plasmin and papain
- polymorphic w/ 13 alloitropes
- heaviest 
- 62 AA and 11 disulfide sodium 
-
A

Lgg3

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56
Q
  • compromises of 5-8%
  • has a major role in immune responses against protein or polypeptide antigens
  • effective in induction of effector fucntions
  • a potent proinflammatory antibody
  • limit excessive inflammation
  • highest C1 and Fc G receptors binding
A

lgg3

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57
Q

this kind of Lgg class

  • heterobivalent
  • fab arm exhange
  • mimic lgg rheutamoid activity
  • regulated by t helper cells
  • allergy diagnosis
  • lessens system inflammatory
A

lgg4

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58
Q

this lgg class
- does not bind
- bind to fcy receptor
- Prominent in the response to therapeutic proteins such as
clotting factor VIII and therapeutic antibodies such as
infliximab (Remicade)

A

lgg4

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59
Q

this immunoglbulin

  • 2nd most abundant isotope
  • 10-15%
  • in tears, mucus, colstrum
  • respi/unri, prostate secretion
A

LgA

60
Q

2 types of LgA

A

Serum IgA

Secretory IgA

61
Q

this lgA

  • does not fix complement
  • lack of complete activation
A

serum lgA

62
Q

this lgA

  • most abundant immuno in mucus secretion
  • confines bacteria to mucosal surface
A

Secretory lgA

63
Q 
this type of LGA 
- -Most important Ig in
human breast milk
-Produced by maternal
plasma cells in the
mammary gland
A

Secretory Lga

64
Q

this tyype of Lga

  • peaks in colstrum
  • remain high till 7 to 8 mos
  • lga high in breast milk
A

secretory lga

65
Q

diseases associated with lga

A

Linear Bullous IgA/Bullous Disease - autoimmune

  • lga nephropathy - glmerular nephritis
66
Q

Increase in IgA diseases

A 
-Systemic Lupus
Erythmatosus
- Rheumatoid Arthritis
-Cirrhosis of Liver
-IgA Myeloma
67
Q

decrease in IgA diseases

A 
-Hereditary Ataxia
Telangiectasia
- Malabsorption Syndrome
- Chronic Lymphocytic
leukemia
68
Q

this type of immuno

  • most heat liable
  • least abundant
  • low concentration of serum
  • 2.5 days half life
  • important defense against parasitic disease by protzoa and helmiths
A

IMMUNOGLOBULIN E

69
Q 
this type of immuno
- have 2 types of receptors 
- › FcεRI: high affinity IgE receptor
› FcεRII (also known as CD23): low affinity
IgE receptor
- does not activate complement
A

IMMUNOGLOBULIN E

70
Q

this type of immuno
- Allergic Manifestations
› self-reactive IgE immune complexes
› IgE’s active basophils

A

IMMUNOGLOBULIN E

71
Q 
function of this immuno 
- type 1 sensitivity 
- protective role by triggering an acute
inflammatory reaction - recruits neutrophils and
eosinophils
- immunity from parasites 
- activates eosinophil
A

IMMUNOGLOBULIN E

72
Q

dieases when increase in lge

A 
Anaphylactic shock
Asthma
Allergic rhinitis
Hypogammaglobulinemia
Atopic skin diseases
Congenital
agammaglobulinemia
73
Q

diseases when decrease in lge

A 
Atopic skin diseases
Congenital
agammaglobulinemia
Allergic rhinitis
Hypogammaglobulinemia
74
Q
  • high levels of lge in the blood
  • stat3 mutation
  • recurrent infections
  • raches, scaling, pus, inflammatory skin disorder
  • open sores
A

Lupus systemic lupus Erythematosuss (SLE)

75
Q

this immunoglobulin

  • unclear function
  • not known to participate
  • low in serum
  • extra AA at C terminal
  • does not bind to complement

loc: surface of b cells

A

LgD

76
Q

diseases in ldg when increases

A

-Atopic Skin
Diseases
-Allergic Rhinitis
-Asthma

77
Q

diseases in ldg when decreases

A

-Hypo gamma globullinemia
- Congenital
A gamma globulinemia

78
Q

some function of microbes

A
  • neutralize toxic material
  • activate complement system
  • immediate hypersensitivity
79
Q

molecular structure of immunoglobulin

A

2 heavy H chains
in heavy Chain - Variable region → 1 Ig domain
b. Constant region → ~3 or 4 Ig domains

2 light chains

  • disulfide bond
  • variable region - binding

Constant region - antibody class

80
Q

forms of antibodies

A
  • Membrane bound

- Secreted antibodies

81
Q

form of antibody that is

  • surface of b lymphocytes
  • receptor for antigens
  • hummoral response
A

Membrane bound antibody

82
Q

form of antibody that is

  • reside in circulation and mucus
  • bind antigen
  • neutralize toxins
  • prevent entry and spread of pathogens
A

Secretory antibody

83
Q

this region

  • shallow crevice in center of hydrophobic core
  • antigen binding site
A

Variable region

84
Q

Fragment Antigen binding

A

Fab

85
Q

complementary determining region

A
  • form a complementary to 3 dimentsional strcuture
  • CDR3 of both VL is most variable to CDrs
  • form extended loops that are exposes on the surface
86
Q
  • area that gives molecule flexibility
  • allow multiple biding sites
  • cleaved papain
  • cleaved pepsin
A

Hinge region

87
Q

3 results fragments from the hinger region

A

2 Fab

1 FC - Fragment crystallizable)

88
Q

G A M E D

arrange from most prominent to least

A

Remember! [G → A→ M → E→D] (most prominent, to

least prominent)

89
Q

Subclasses / subtypes: in the Constant region

A

IgA – IgA1, IgA2

IgG – IgG1, IgG2, IgG3, IgG4

90
Q

What transpires in the Constant region?

A 
Agglutination
● Complement Fixation
● Antigen attachment (for opsonization)
● Ab-dependent cell cytotoxicity (ADCC)
● Viral neutralization
91
Q

What transpires in the Constant region?

A 
Agglutination
● Complement Fixation
● Antigen attachment (for opsonization)
● Ab-dependent cell cytotoxicity (ADCC)
● Viral neutralization
92
Q

what is the longest

A

Lge

93
Q

heavy chains C region

A

CH

94
Q

how many tandems does CH contain in humans

A

4 tandems lg domain

Designated CH and numbered sequentially from
amino terminus to carboxyl terminus (eg. CH1,
CH2 and so on)

95
Q

composition of light chains

A

2 Identical Light Chains (L Chain)
- L chain - half of H chain
› 2 identical heavy chains (H chain) in most IgS
- H chain – 440 amino acids (50 kDa)

Covalent linkage by disulfide bonds between

96
Q

have the shortest H chains

A

Lgs

97
Q

= variable region

A

Half of light chain toward carboxyl terminal (COO-) =

constant region; amino terminal half

98
Q

all light chains are either

A 
either kappa (κ) or lambda (λ) type
(NEVER A MIXTURE) based on their C regions
99
Q

what chains are frequent in the humans

A

Kappa K chains

100
Q

what determines lg class and effecter

A

tyype of h chains

101
Q

types of H chains

A 
IgG γ – gamma
IgA α – alpha
IgM μ – mu
IgE ε – epsilon
IgD δ – delta
102
Q

no 2 variable regions are identical

A

L chains – 3

› H chains – 4

103
Q

I. TWO PRIMARY FUNCTION OF IGs

A
  1. Antigen recognition
    - Recognize and bind an enormous variety of antigenic
    determinants
  2. Effector functions
    -Mediate the biologic effects of immunoglobulin
104
Q

is a foreign substance that includes
antibody and/or CMI after binding to its specific
antigenic receptor on T and B cell clones.

A

ANTIGEN

105
Q

Specificity for binding an epitope of an

antigen (epitope – T cell receptor response)

A

Fab portion

106
Q

› Directs the biological activity

A

Fc Portion

107
Q

lock and key concept

A 
Ag = Key
Ab = Lock
108
Q

constructed from the
hypervariable regions of the heavy and light
chains

A

Combining site

109
Q

what happens in the fab portion combing site

A

(Ag) and antibodies (Ab) interacting shows
that the antigenic determinant nestles in a
cleft

110
Q

these binds hold the AG
ex. hydrogen bond
vander waals

A

non covalent bonds

111
Q

Ag-Ab reactions occur via non-covalent bonds

A

REVERSIBLE BONDING

112
Q

functions of the effector

A
  • neutralize toxic microbes
  • complement system activation
  • opsonization
  • hypersensitivity
  • H chain determines class
    c region in FC defines effector funtion of specific lg
113
Q

what can synthesize antibody molecules

A

Only B lymphocytes

thru fluids in the body

114
Q

Strength of reaction between single antigenic determinant
and a single combining site on antibody

Strength of reaction of 1 antigen to antibody

A

AFFINITY

115
Q

overall strength of binding of an antigen with

many antigenic determinants and multivalent antibodies

A

AVIDITY

116
Q

more than one antigenic determinant

ability of ab to react to more than one ag

A

cross reactivity

117
Q

FEATURES RELATED TO ANTIGEN-

ANTIBODY INTERACTION

A

Specificity
● Cross Reaction
● Diversity
● Affinity Maturation

118
Q

You only have 1 antigen-antibody

reaction

A

Specificity:

119
Q

Antibody fits with antigen because
of shared epitope. Antibody still slightly fits because of
similar epitope.

A

Cross reaction:

120
Q

the part of the antigen that binds to a specific antigen receptor on the surface of a B cell.

A

epitope

121
Q

factors affectting the measurement of antigen antibodyy

A

Affinity & avidity

Antigen-antibody ratio

122
Q

Physical form of the antigen if antigen is:

A

particulate

soluble

123
Q

precipitation of the antigen after the production of

large insoluble Ag/Ab complexes

A

soluble

124
Q

agglutination of antigen by antibody

A

particulate

125
Q

Ability to respond to antigens that are “foreign” or non-self,
and to not respond to antigens that are self

A

hummoral infinity

126
Q

ability to recall previous contact with a particular

antigen so that a subsequent interaction leads to a quicker,

A

memory

127
Q

vaccine types

A

Toxoid vaccines
Killed vaccines (e.g.
Live attenuated

128
Q

Live attenuated vaccine ex

A

mmr and varicella vaccine

129
Q

Killed vaccines ex

A

inactivated polio vaccine [IPV])

130
Q

Toxoid vaccines ex

A

diphtheria & tetanus

131
Q

first arrangement of lg genes
Dh to h chain gene
- CD10 and CD19

A

Pro B cell

132
Q

2nd arrangement

Vdj recombinase joins heavy

A

pre cell b

133
Q

Light chains are paired with μ chains to form monomeric IgM
which is expressed in the cell surface to form B cell receptor

CD20 – marks late stage development of B cell
› CD10: from pro-B to pre-B cell only

A

Immature B Cell

134
Q

1st stage in B cell differentiation pathway to express receptor
(B lymphocyte factor which belongs to the tumor necrosis

no encountered antigen

A

Transitional B Cell

135
Q

Monomeric IgM and IgD on the surface of B cell

naive cells

A

Mature B Cell

136
Q

B cells not yet exposed to antigen
› Exposure to antigen in secondary lymphoid tissue
results in activation, leads to formation of either
plasma cell or memory cell

A

naive B cells

137
Q

can synthesize and secrete lg molecule

Do not express surface Ig

A

Plasma Cell

138
Q

key part of the innate immune system that enhances the
antibody-mediated adaptive immune system and its response
to microbial pathogens

A

complement system

139
Q

major function

A

cell lysis
opsonization
C3b

140
Q

most important opsonizing activity

A

CB3

complement 3

141
Q

proteins are inactive complement system

what activates proteins

A

biochemical cascade pathways that

sequentially generates biologically active molecules

142
Q

Activation pathways:

A

Classical, Alternative, Lectin/

Mannose-binding lectin (MBL)

143
Q

Deficiencies of complement components, regulators, or
receptors may result in increased susceptibility to infection
or the development of inflammatory conditions

A 
important complement functions
› Enhancement of B-cell responses
› Removal of immune complexes
› Removal of necrotic cells and subcellular membranes
› Responses to viruses
144
Q 
activated by antigen antibody complex
- initiated by lgg or lgm 
- fc part of bind site 
lgg phagocytic 
- opsonization
A

classical pathway

145
Q
  1. C1q binds to Fc region of antibody bound to antigen C1
    becomes activated. (C1 exists in blood and contains C1q, r, s)
    1. C1s esterase cleaves C4 molecules C4a (smaller) and
      C4b (larger)
      › C4a remains in fluid
      › C4b binds to pathogen
  3. C4b binds C2 then it cleaves it into C2a and C2b
  4. C2a binds with C4b to form C4b2a complex which is a
    protease known as (C3 convertase)
A
  1. C3 convertase cleaves C3 into C3a and C3b
    › C3a is a chemoattractant, it recruits leukocytes to
    infection
    sites to stimulate inflammatory response
    › C3b binds with C3 convertase
  2. C3a binds with C2a and c4b fragments to form a complex
    known as (C5 convertase)
  3. C5 convertase cleaves C5 into C5a and C5b
    › C5a is a chemoattractant just like C3a
  4. C5b combines with C 6, 7, 8, 9 to form membrane attack
    complex (MAC)
    MAC kills bacterial invaders by binding to and opening a pore
    in their plasma membrane. Following lysis, the bacterial
    remains are destroyed by phagocytic macrophages.
146
Q
  • triggered by any foreign substance in the absence of specific antibody
  • key role in innate immune system
    early response
A

alternate pathway

147
Q
  1. Deposition of C3b on the cell surface
    › C3b is generated in small amounts by the spontaneous
    cleavage of the reactive thiol group in C3
    › “Preformed” C3b can bind to proteins and carbohydrates
    expressed on cell surfaces, either of a pathogen or of a
    host cell
    › Alternative pathway is always “on” → can damage host
    cells
    › Host cell - regulates the progression of alternative
    Pathway
A
  1. Serum protein factor B binds with C3b → form C3bB
    complex
  2. Factor D cleaves factor B → generating fragments Ba and
    Bb
    › Ba - released into the fluid phase
    › Bb - remains attached to C3b
    › Formation of C3bBb - C3 convertase in the alternative
    pathway
  3. Shares the same steps (5-8) as the classical pathway

Module 5 Hematology (4 decks)

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