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1 STEP Uworld immunology > Immunology > Flashcards

Immunology Flashcards

1
Q

What effect may cause high doses of corticosteroids on nerve system?

A

corticosteroid-induced psychosis (hallucinations, confusion)

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2
Q

What is the acute effect of corticosteroids on WBCs? (5)

A

Incr. neutrophils, decr. basophils, eosinophils, monocytes, lymphocytes

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3
Q

Corticosteroid use –> dec. basophils. Effect? Why?

A

decreased local inflammatory responses by preventing histamine release.

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4
Q

Corticosteroid use –> dec. eosinophils. Effect? Why

A

reduced eosinophil count –> decreased mediators release from eosinophils in allergic reactions.

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5
Q

Where corticosteroids redistribute lymphocytes from vessels? (3)

A

spleen, lymph nodes, bone marrows

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6
Q

When corticosteroid use -T or B lymphocytes decr. more?

A

T lymphocytes

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7
Q

how corticosteroids decreased lymphocytes?

A

inhibit Ig synthesis + stimulate lymphocyte apoptosis + redistribute lymphocytes to lymphoid organs

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8
Q

Corticosteroid use –> effect on macrophages?

A

inhibit peripheral extravasation

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9
Q

What is the effect of corticosteroids on the presentation of the antigen?

A

presentation is decrease by macrophages and dendritic cells

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10
Q

T-lymphocytes, or thymocytes, are produced in the bone marrow and undergo maturation in the thymus during ……………….

A

the first trimester of gestation

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11
Q

Procesess of TCR in thymus (4)

A

beta gene rearragement –> alpha gene rearrgament –> positive selection –> negative selection –> expression of membrane markers and co-stimulatory molecules

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12
Q

What means ,,double negative” T lymphocyte?

A

Lack of both CD4 and CD8

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13
Q

What is maturation of T lymphocyte?

A

loss of either CD4 or CD8, because as a result it has to have only one marker

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14
Q

Thymic epithelial cell express …………..

A

MHC antigens

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15
Q

Thymic epithelial cell express interact with ……… lymphocytes

A

immature

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16
Q

what happens if lymphocyte in positive selection stage cannot bind thymic receptors?

A

Are killed or becomes regulatory

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17
Q

What T cells can be activated by dendritic cells?

A

All types - naive, effector and memory

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18
Q

What’s the different between dendritic and macrophages/pagocytes in regard of MHC II?

A

Dendritic - express constitutively

Macrophages - inducably

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19
Q

What T cells can be activated by macrophages?

A

effector and memory [NO NAIVE}

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20
Q

What T cells can be activated by B cells?

A

All types - naive, effector, memory

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21
Q

How B cells express MHC II?

A

Constitutively (are always “on”)

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22
Q

What 2 tests measure the function of the complement?

A

CH50 (total complement)

AH50 (alternative pathway)

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23
Q

Deficiency in the terminal pathway (C3; C5-C9). CH50 and AH50 levels?

A

Low, low

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24
Q

Lectin complement deficiency? CH50 and AH50 levels?

A

Normal, normal

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25
Q

Classical cascade deficiency? CH50 and AH50 levels?

A

Low and normal

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26
Q

Alternative pathway factor B and D deficiency. CH50 and AH50 levels?

A

Normal, low

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27
Q

What are steps of leukocyte adhesion cascade?

A

Margination, rolling, activation, tight adhesion, transmigration

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28
Q

What increases expression of endothelial selectins? what step?

A

cytokines; rolling

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29
Q

What facilitates margination of lymphocytes?

A

hemoconcentration and decreased wall shear

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30
Q

LAD 2 damage in which lymphocyte adhesion step?

A

Rolling

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31
Q

What components are on the neutrophils and endothelial cells in the rolling step?

A

Neutrophils - sialylated carbohydrate groups (Sialyl Lewis X or PSGL-1)
Endothelial cells - L-selectin or E/P-selectin

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32
Q

LAD3 defect, what adhesion step?

A

Activation

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33
Q

why slow rolling of neutrophils is important?

A

neutrophils can sample cytokines from inflammed tissue which cause conformational changes in integrins needed for binding.

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34
Q

In which stage neutrophils become firmly attached to the endothelium?

A

Tight adhesion and crawling

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35
Q

Junction of neutrophils and endothelial cells in tight adhesion and crawling?

A

Neutrophils - CD18 beta 2 integrins (mac1 and LFA1)

Endothelial - ICAM1

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36
Q

What is CD18 beta 2 integrins (mac1 and LFA1)?

A

junction molecules on neutrophil to bind ICAM1 and endothelial cell. Tight adhesion and crawling step

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37
Q

Where is found PECAM1?

A

at the peripheral intercellular junctions of endothelial cells.

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38
Q

LAD 1 defect which step?

A

Tight adhesion

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39
Q

In rolling stage participate ……………..; in activatio - ……….

A

cytokines; chemokines

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40
Q

What do cytokines in leukocyte adhesion process?

A

Induce endothelial expression of selectins

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41
Q

What do chemokines?

A

lead to integrin activation

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42
Q

Inheritance of LADs?

A

autosomal recessive

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43
Q

LAD type 1 results from ………

A

absence of CD18

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44
Q

recurren skin infections without pus + poor wound healing + delayed umbilical deatachment = ?

A

LAD 1

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45
Q

LAD 1 leads to inability to sinthesize ……….

A

beta2 integrins Mac1 and LFA1

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46
Q

In LAD 1 are affected …… steps.

A

tight adhesion and crawling + trasmigration

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47
Q

What is the difference in LAD1 and LAD2 in clinical manifestation?

A

LAD 1 more severe. LAD2 has no delay in umbilical cord separation and less sever and fewer infections.

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48
Q

What is the similarities and diffecences in LAD1 and LAD3?

A

same clinical manifestaion: severe recurrent infections, delayed umbilical separation; dif - bleeding complications due to affected beta 3 integrins on patelets.

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49
Q

Which LAD manifest as bleeding?

A

LAD3

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50
Q

IgG primarily is responsible for …….

A

recurrent bacterial infections

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51
Q

Ig region that activates complement?

A

Fc - CH2 (second heavy chain)

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52
Q

Which complement is activated by IgG?

A

Classical

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53
Q

2 mechanisms of action by IgG?

A

Complement activation and direct phagocytosis

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54
Q

Direct phagocytosis by IgG. What part of Ig is ligand for phagocytic cell? What part of p.cell binds?

A

Fc, third heavy chain.

p.cell - Fc receptor (CD16)

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55
Q

Lymph nodes serve as sentinel sites for generation of ……………

A

the adaptive immune response

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56
Q

What cells display large, unprocessed foreign antigen to draining lymph node?

A

follicular dendritic cells

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57
Q

Which part of lymph nodes get large, unprocessed antigent?

A

B cells germinal centers

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58
Q

Who process large antigen to small in lymph node?

A

B cells

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59
Q

What happens when B cells display small antigen parts to MHC II to naive T?

A

Naive T cells differentiate to helpers –> secretion of cytokines

60
Q

What do cytokines produced by T cells in lymph nodes?

A

promote survival and proliferation of the ANTIGEN SPECIFIC B CELLS –> leads to generation of germian centers.

61
Q

Why in malignancy there is no pain in lymph nodes?

A

Because (in case of atypical B cells) proliferation of B cells without antigen stimulation is not assoc. with cytokine release.

62
Q

What changes (histo) happens in bacterial infection in lymph node?

A

FORMATION OF GERMINAL CENTERS

63
Q

Chemotactic agents? (4)

A

leukotriene B4, 5-HETE, C5a, IL-8

64
Q

Why there is protein-reach exudate in inflammatory site?

A

Due to increased vascular permeability

65
Q

Autoimmune hepatitis. Antibodies?

A

Smooth muscle cell antibodies

66
Q

Primary biliary cholangitis. Antibodies?

A

Antimitochondrial antibodies

67
Q

What target c-ANCAs?

A

neutrophil proteinase 3

68
Q

wegener (granulomatosis with polyangiitis) antibodies?

A

c-ANCA

69
Q

What signaling is in interferon pathway?

A

autocrine/paracrine

70
Q

What receptors bind interferons on infected cells?

A

Type I interferon receptors

71
Q

What happens when interferons reach neighboring cells?

A

induce transcription of antiviral enzymes

72
Q

What is the function of antiviral enzymes?

A

halting protein synthesis of virus

73
Q

What proteins produce virally infected cells?

A 
RNase L (endonuclease that degrades all RNA in the cell)
Protein kinase R (inactivates eIF-2, which inhibits translation initiation)
74
Q

What do RNase L?

A

Endonuclease that degrades all RNA in the cell

75
Q

What do protein kinase R?

A

Inactivates eIF-2, which inhibits translation initiation

76
Q

What condition is needed to make active RNase L and Protein kinase R?

A

double-stranded RNA [viral made]. Must to be, othervise enzymes won’t be active

77
Q

What forms in the cell of viral replication?

A

double-stranded RNA

78
Q

interferons induce expression on the cell surface ………

A

MHC I

79
Q

What type interferon in INF gama?

A

type I

80
Q

3 functions of interferon gama?

A

promotes Th1 differentiation
incr. MHC II expression on APC
improves intracellular ability of marcophages

81
Q

Absence of HLA-DR indicates …..

A

defective expression of MHC II

82
Q

MHC I present after antigen …..

A

cytosolic antigent presented to endoplasmic reticulum

83
Q

MHC II present after antigen …….

A

endocytosis with acidified lysosome

84
Q

How interferon gamma improves antigen presentation?

A

increases expression of MHC I and II

85
Q

What enzymes induce apoptosis?

A

granzymes, perforins

86
Q

TAP is related to which antigen-presenting receptor?

A

MHC I

87
Q

TAP allows to present antigen from …….. to ………

A

cytosol to ER

88
Q

Viral infection. MHC I has antigen. What happens next?

A

Antigen is presented to cytotoxic T cells to TCR and CD8

89
Q

What part of Ig makes them susceptible to proteases? Which Ig has it?

A

hinge region;

IgG, IgD, IgA

90
Q

What is advantages of having hinge region?

A

Increased flexibility –> Increased avidity (IgA, IgG, IgD)

91
Q

IgE interacts with the ………. receptor on ……………

A

Fc epsilon; mast cells

92
Q

IgG interacts with the ………

receptor on …….. and ……..

A

Fc gamma; phagocytes/NK cells

93
Q

IgA interacts with the ……… receptor on …………., ……………, and ………..

A

Fc alpha; neutrophils, macrophages, and eosinophils.

94
Q

What helps to IgA and IgM to become multimers? (2)

A

disulfide bonds between Fc chains and additional amino acid sequence called J chain

95
Q

What’s the point of hinge region?

A

flexibility to Fab arms

96
Q

Longer hinge regions are associated with ……………. Why?

A

increased antibody avidity; Fab can reach antigens that are farther apart on the bacteria

97
Q

What Ig do not have hinge?

A

IgE and IgM

98
Q

Which Ig is longer?

A

IgM

99
Q

Where phagocytic cells bing IgM?

A

CH4

100
Q

Hinge region is rich in ………………… and ……….

A

cysteine and proline

101
Q

Disadvantage of hinge region?

A

susceptability to proteases

102
Q

Affinity vs avidity?

A

affinity –> stronger single connection; avidity –> bond more antigens

103
Q

FOXP3 encodes a transcriptional regulator that converts ……………… into ………….

A

activated CD4 into T reg

104
Q

What is the function of T reg?

A

Inhibit immune activation

105
Q

Expression of FOXP3 drives production of … (3)

A

it activates cytotoxic T CD 4 and it leads to synthesis of IL-10; TGFbeta

106
Q

3 functions of IL-10?

A

inhibits macrophages; downregulates MHC II on APCs; block inflamatory cytokine release from T CD4

107
Q

2 functions of TGF-beta?

A

inhibits B-lumphocyte proliferation/activation;

promotes Treg differentiation (eg FOXP3 expression)

108
Q

FOXP3 –> cytotoxic CD4. Role?

A

Cytotoxic –> CD4 binds B7 on APC –> less available APC to bind T cells –> less active T cells

109
Q

Reason if IPEX?

A

mutation in FOXP3

110
Q

IPEX manifestation (3)

A

autoimmune enteritis; eczematous dermatitis; DM1

111
Q

Inflammatory reaction that occurs shortly after vaccination

A

reactogenicity

112
Q

What immune system part is activated in case of acute onset symptoms after immunization?

A

rapid-onset innate immune response

113
Q

What drives rapid-onset innate immune response?

A

pattern recognition receptors on local stromal and local/circulation immune cells (eg marcophages, monocytes, mast cells)

114
Q

Activated pattern recognition receptions recognize ……………… and it results in ………………………..

A

eg LPS; release of pyrogenic cytokines

115
Q

However, manifestations of reactogenicity tend to improve after ……….

A

24-36 hours after vaccination

116
Q

Immune checkpoint receptor? What it binds?

A

CTLA4; CD80/86

117
Q

MHC I is decreased in …. (2)

A

Virus-infected and tumor cells

118
Q

What facilitates granzymes gain access in target cells?

A

Perforins make holes in the membrane and granzymes via it enters the cell.

119
Q

Function of perforins?

A

produce holes in cell membrane

120
Q

Function of granzymes?

A

induce cell apoptosis

121
Q

What is the result of NK cells function on cells?

A

Target cell undergoes apoptosis.

122
Q

What surface markers express NK cells?

A

CD16 and CD56

123
Q

In athymic patients there is a lack of T lymphocytes, but not ……., because they do not mature in thymus.

A

NK cells

124
Q

What activates NK cells? (2)

A

INF gamma and IL-12

125
Q

There is antigen in intestinal mucosa. What happens firstly?

A

B cells move from mesenteric lymph nodes and peyer’s patches to lamina propria uderlying the intestinal mucosa.

126
Q

Where B cells become fully differentiated in gut?

A

In lamina propria underlying the intestinal mucose

127
Q

What bing IgA in mucose after they are synthesized?

A

pIgR - polymeric immunoglobulin receptor

128
Q

Where is found pIgR?

A

basolateral surface of intestinal epithelial cells

129
Q

What happens to pIgR after IgA is secreted to intestinal lumen?

A

part is left in endosome where IgA and pIgR was, other part is left attached to IgA and is called secretory component.

130
Q

Why in hyper IgM syndrome patients are prone to have sinopulmonary recurrent infections?

A

Lack of IgG –> no opsonization

131
Q

Why in hyper IgM syndrome patients are prone to have GI infections?

A

Lack of IgA

132
Q

Why in hyper IgM syndrome patients fail to thrive?

A

increased metabolic demands from recurrent infections, as well as nutrient loss from chronic diarrhea

133
Q

2 functions of ROS?

A

direct damage to m/o

activate granule proteases

134
Q

What enzyme is increased in anaphylaxis?

A

tryptase

135
Q

triad of dead due to anaphylaxis

A

Laryngeal edema + hyperinflated lungs + cerebral edema

136
Q

Why there is hypotension in anaphylaxis?

A

histamine –> H1 and H2 receptors –> vasodilation

137
Q

Why there is tachycardia in anaphylxis?

A

histamine –> H1 and H2 receptors –> inc. catecholamine secretion.
dar bus del hypotension

138
Q

Why there is bronchoconstriction in anaphyaxis?

A

Histamine –> H1 receptors

139
Q

Why there is incr. vascular permeability in anaphylaxis?

A

Histamine –> H1 receptors

140
Q

Why there is GI symptoms in anaphylaxis?

A

Histamine –> H2 receptors –> incr. gastric acid secretion –> contributes symptoms such vomiting, nausea

141
Q

Why there is pruritus/pain in anaphylaxis?

A

histamine activate nociceptive receptors

142
Q

histologic examination of acute serum sickness? (2)

A

small vessel vasculitis with fibrinoid necrosis and intense neutrophilic infiltration

143
Q

which complement is decreased in type 3?

A

C3

144
Q

why neutropenia may manifest in serum sickness?

A

serum sickness –> release of C5 = neutrophilic attachement at the site on complex deposition –> neutrophilic marginalization and tissue infiltration

145
Q

WHy may manifest thrombocytopenia in serum sickness?

A

active vascular inflmmation –> local platelet consumption –> mild thrombocytopenia

146
Q

what is the difference between DIC and henoch schonlein purpuros? pathohistology

A

DIC - fibrin deposits, no vascular inflammation

HSP - may be seen fibrin thrombi, extensive vascular inflammation

1 STEP Uworld immunology (13 decks)

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