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Immunology Flashcards

1
Q

Medulla of lymph node

A

Medullary cords with closely packed lymphocytes and plasma cells

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2
Q

Medullary sinuses

A

Contain reticular cells and macros communicate with efferent lymphatics.

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3
Q

paracortex

A

Houses T cells. Between cortex between follicles and medulla. High endothelial venules

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4
Q

Which part of lymph node enlarged in immune response?

A

paracortex. This part is also underdeveloped in digeorge syndrome

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5
Q

stomach drains to

A

celiac node

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6
Q

duodenum drains to

A

superior mesenteric node

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7
Q

sigmoid colon drains to

A

colic then inferior mesenteric

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8
Q

rectum drains to

A

internal iliac nodes

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9
Q

anal canal below pectinate drains to

A

superficial inguinal

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10
Q

testes drain to

A

superficial and paraaortic

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11
Q

scrotum drains

A

superficial inguinal node

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12
Q

thigh drains

A

superficial inguinal node

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13
Q

lateral dorsum of foot drains

A

popliteal

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14
Q

right lymphatic duct drains

A

right arm, right chest, right half of head

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15
Q

thoracic duct drains

A

everything beisdes what the right lymphatic duct drains

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16
Q

structure of sinusoids of spleen

A

vascular channels in red pulp with barrel hoop basement membrane

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17
Q

T cells of spleen found in

A

periarterial lymphatic sheath in white pulp

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18
Q

B cells of spleen found in

A

follicles on outer edge of white pulp

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19
Q

Macrophages of spleen are especially important for

A

removing encapsulated bacteria

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20
Q

What are the encapsulated organisms?

A 
Strep
HiB
Neisseria
Salmonella
Klebsiella
Group B
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21
Q

Findings in a blood smear after a splenectomy

A

howell jolly bodies
target cells
thrombocytosis

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22
Q

Cortex of thymus

A

immature T cells

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23
Q

medulla of thymus

A

pale with mature T cells

epithelial reticular cells coming together to make hassall’s corpuscles

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24
Q

positive selection (MHC restriction) occurs

A

in the cortex of thymus

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25
Q

negative selection (nonreactive to self) occurs

A

in the medulla of thymus

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26
Q

MHC I is expressed on all nucleated cells except for

A

RBCs

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27
Q

B2 microglobulin

A

part of MHC1, helps to transport molecule to cell surface

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28
Q

loading of antigen in MHC II

A

release of invariant chain in acidified endosome

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29
Q

loading of antigen in MHC1

A

in RER with intracellular peptides

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30
Q

HLA A3

A

hemochromatosis

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31
Q

HLA DQ2/DQ8

A

celiac

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32
Q

HLA DR2

A

multiple sclerosis
SLE
Goodpasteur’s

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33
Q

HLA DR3

A

Graves’ Diabetes type 1

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34
Q

HLA DR4

A

rheumatoid arthritis, diabetes type 1

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35
Q

HLA DR5

A

pernicious anemia

Hashimoto’s thyroiditis

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36
Q

when do NK cells kill?

A

Exposed to a nonspecific activation signal on target or absence of class I MHC

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37
Q

NK activity enhanced by

A

IL-2, IL-12, IFN beta, IFN a

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38
Q

When an immature T cell enters the thymus, it immediate gets what receptors?

A

CD4+ CD8+ AND TCR

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39
Q

SIgnal for Helper T cells to become Th1 cells

A

IL-12

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40
Q

Signal for helper T cells to become Th2 cells

A

IL-4

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41
Q

Positive selection

A

T Cells expressing TCRs able to bind self MHC survive

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42
Q

negative selection

A

T cells expressing TCRs with a high affinity for self antigens= apop

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43
Q

costimulatory signal

A

B7 expressed by DC

CD28 expressed by naive T cell

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44
Q

What happens after the primary and costimulatory signal is given by dendritic cell to naive T cell?

A

Naive T cell expresses IL-2 which binds to IL-2R on itself stimulating the naive T cell to differentiate

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45
Q

What happens after the primary and costimulatory signal is given by Th4 cell to naive B cell?

A

the helper T cell, after being activated by dendritic cell

  • ->B cell presents antigen on MHC II to activated T cell
  • ->TCR recognizes correct antigen and releases IL4 and IL5 which stimulate the B cell to differentiate into IgG, IgE, and IgA
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46
Q

What is the only APC that can activate a naive T cell?

A

the dendritic cell

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47
Q

Describe the costimulatory signal for B cell activation

A

CD 40 on B cell

CD40 L on Th cell

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48
Q

Th1 cell secretes

A

IFN-y

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49
Q

Th2 cell secretes

A

IL4, 5, 10, 13

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50
Q

Th1 cell activates

A

macrophages

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51
Q

Th2 cell activates

A

Eosinophils

IgE production by B cells

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52
Q

Th1 cell inhibited by

A

IL4 and IL10

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53
Q

Th2 inhibited by

A

IFN-y

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54
Q

How do macrophages and lymphocytes tickle or stimulate each other?

A

lymphocytes release IFN-y
macrophages release IL1 and TNF-a
–> they help each other out

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55
Q

Hyper IgM caused by

A

Defective CD 40 and 40L interaction

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56
Q

Contents of cytotoxic T cells (CD8)

A

granules with

  1. perforin: makes holes so can deliver bombs
  2. granzyme: serine protease, activates apoptosis
  3. granulysin: antimicrobial, induces apoptosis
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57
Q

Treg cells express which cell surface markers

A

CD3, CD4, and CD25

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58
Q

Treg cells produce

A

IL10 and TGFbeta

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59
Q

heavy chain makes up which portions of antibody

A

Fc and Fab

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60
Q

light chain makes up which portion of antibody

A

Fab

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61
Q

CD25 is also known as

A

alpha chain of IL-2 receptor.

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62
Q

complement binds which part of antibody

A

medial portion of Fc

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63
Q

macrophage binds which part of antibody

A

distal to where complement binds, between CH2 and CH3

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64
Q

three components of the Fc region

A

carboxyterminal end
complement binding at CH2 (IgG and IgM)
Carbohydrage side chains

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65
Q

light chains made up of

A

VJ

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66
Q

heavy chains made up of

A

VDJ

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67
Q

stomatic hypermutation occurs after

A

antigen stimulation of B cell. BUT B cells are “born” with their random VJ/VDJ combinations.

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68
Q

What enzyme is responsible for generating the VD/VDJ recomination?

A

terminal deoxynucleotidyl transferase

–Adds nucleotides to DNA during recombination

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69
Q

isotype switching

A

When B cells secrete things other than IgM

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70
Q

Mature B lymphocytes express what on their surface

A

IgM AND IgD

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71
Q

Which antibody can cross the placenta?

A

IgG

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72
Q

Which antibodies can fix complement?

A

Only IgG and IgM

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73
Q

which antibody is responsible for delayed response to an antigen?

A

IgG

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74
Q

How does IgA work?

A

Prevents attachment of bacteria to mucous membranes

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75
Q

IgA form in circulation?

A

monomer. dimer when secreted

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76
Q

Which Ig is the antigen receptor of the surface of B cells?

A

IgM

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77
Q

thymus independent antigens

A

antigens lack a peptide component and cannot be presented by MHC to T cells (ex: LPS or capsular antigen)

  • ->as a result, NO immunologic memory
  • ->but antibodies are released
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78
Q

Thymus dependent antigens

A

There IS a protein component (diptheria) and class switching occurs

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79
Q

Classic complement pathway

A

IgG or IgM mediated

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80
Q

Lectin pathway

A

mediated by Mannose on microbe

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81
Q

Alternative pathway turned on by

A

PAMP pathogen associated molecular pattern

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82
Q

C3b

A

opsonization

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83
Q

C5a

A

neutrophil chemotaxis

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84
Q

What starts the alternative pathway?

A

C3–>C3b
AND
D converts B into Bb
=C3bBb

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85
Q

what starts the lectin pathway?

A

MBL activates a C1 like complex

  • -cleaves C2 AND C4
  • -otherwise, same as classic pathway
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86
Q

primary opsonins

A

IgG

C3b

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87
Q

What prevents complement activation on self cells?

A

Decay accelerating factor

C1 esterase inhibitor

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88
Q

complement disorder with hereditary angioedema

A

C1 esterase inhibitor deficiency

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89
Q

What drug is contraindicated in C1 esterase inhibitor deficiency?

A

ACE inhibitors

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90
Q

severe pyogenic sinus and respiratory tract infections with increased type III hypersensitivity–type of complement deficiency

A

C3 deficiency. C3 helps clear immune complexes

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91
Q

Recurrent neisseria bacteremia

A

C5-9 deficiency

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92
Q

Complement mediated lysis of RBCs and PNH

A

DAF deficiency

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93
Q

What does IL-1 do to endothelium?

A

induces adhesion molecule expression

94
Q

IL6

A

fever and acute phase proteins

95
Q

IL8

A

neutrophil chemotaxis

96
Q

IL12

A

Differentiation into Th1 cells

Activates NK cells

97
Q

IFN-y

A

Increase MHC I and II expression.

98
Q

Interferon a and b mechanism

A

Produce a ribonuclease=degradation of viral mRNA

99
Q

IFN is defense against

A

VIRUSES

–they all activate NK cells to kill virus infected cells

100
Q

Cell surface proteins on T cells

A

TCR
CD3
CD28

101
Q

CD proteins on Th4

A

CD4, CD40L

102
Q

B cell CD proteins

A

CD19, 20, 21

40, MHCII, B7

103
Q

Receptor for epstein barr virus

A

CD21

104
Q

Macrophage receptors

A

CD14 (binds LPS)
CD40
MHC II
B7

105
Q

NK cell receptors

A

CD16 (binds Fc)

CD56 (unique marker)

106
Q

Superantigens secreted by which bugs?

A 
S aureus (TSST-1)
S pyogenes (exotoxin A)
-->NOTE THAT ALL T CELLS ARE ACTIVATED from cross linking fo TCR to MHC II on APCs
107
Q

LPS stimulates

A

macrophages!

Thelper cells are NOT involved. Massive secretion of TNF alpha

108
Q

Salmonella antigen variation

A

flagella

109
Q

neisseria gonorrhea antigen variation

A

pilus protein

110
Q

what other bugs have antigen variation?

A

trypanosomes

borrelia

111
Q

When do you give passive immunization?

A

Tetanus
Botox
Rabies
HBV

112
Q

Live vaccines activate a

A

cellular response

113
Q

killed vaccines activate a

A

humoral immunity

114
Q

examples of killed vaccines

A 
Rabies
Influenza (shot)
Polio (salk)
HAv
Cholera
115
Q

marker of mast cell degranulation

A

tryptase

116
Q

Explain Type II hypersensitivity

A

IgM/G bind to antigen

  • -opsonization
  • -complement lysis
  • -Antibody dependent cell mediated cytotoxicity, NK cells
117
Q

How to test for type II hypersen

A

Direct and indirect coombs’

118
Q

serum sickness

A

immune complex disease where immune complexes bind and deposit where they fix complement=tissue damage

119
Q

arthus rxn

A

Intradermal injection induces antibodies and complexes in the skin.
—edema, necrosis, activation of complement

120
Q

When would you see serum sickness?

A

5-10 days after exposure

121
Q

most serum sickness is caused by

A

drugs

122
Q

Sx: serum sickness

A

fever, urticaria, arthralgias, protienuria, lymphadenopathy

123
Q

Test for arthus rxn

A

immunofluorescen staining

124
Q

Describe process of type IV hypersensitivity

A

t lymphocytes activate macrophages and secrete lymphokines

125
Q

Examples of type IV hypersensitivity

A 
multiple sclerosis
guillain barre
graft versus host disease
contact dermatitis
tranplant
TB skin test
126
Q

allergic rhinitis and hay fever

A

Type I hypersensitivity

127
Q

Four types of blood transfusion reactions

A

allergic rxn
anaphylactic
febrile nonhemolytic
acute hemolytic transfusion

128
Q

concern when giving blood transfusion to pt with celiac’s

A

many celiac’s pts are deficient in IgA

–must receive blood products that lack IgA

129
Q

Febrile nonhemolytic transfusion rxn

A

type II hypersensitivity. Host antibodies against donor HLA antigens

130
Q

sx of febrile nonhemolytic TR

A

fever, chills, flushing

131
Q

Acute hemolytic transfusion rxn

A

type II hypersensitivity. Intravascular hemolysis or extravascular hemolysis

132
Q

Sx of acute hemolytic transfusion rxn

A

fever, hemoglobinemia, jaundice (extravascular)

flank pain, hypotension

133
Q

Anti-histone antibody

A

Drug induced lupus

134
Q

anticentromere

A

CREST

135
Q

antiScl70 (DNA topo I)

A

Diffuse scleroderma

136
Q

antimitochondrial

A

primary biliary cirrhosis

137
Q

IgA antiendomyseal

A

celiac

138
Q

anti-desmoglein

A

pemphigus vulgaris

139
Q

antimicrosomal

A

hashimotos

also antithyroglobulin

140
Q

Anti Jo-1, Anti-SRP, Anti-Mi2

A

polymyositis

dermatomyositis

141
Q

Anti-SSA/SSB

A

sjogren

142
Q

anti-smooth muscle

A

autoimmune hep

143
Q

anti glutamate decarboxylase

A

t1D

144
Q

p-ANCA

A

microscopic polyangiitis, churg strauss

145
Q

c-ANCA

A

granulomatosis with polyangiitis

146
Q

anti-glutamate decarb

A

type 1 diabetes

147
Q

anti-U1 RNP

A

mixed CT disease

148
Q

No B cells: susceptible to which bacteria?

A

Encapsulated

149
Q

No complement: susceptible to which bacteria?

A

Neisseria

150
Q

No granulocyte: susceptible to which bacteria?

A

Staph
Serratia
Nocardia

151
Q

No T cells: susceptible to what bacteria?

A

everything. Sepsis!

152
Q

No T cells, susceptible to which viruses?

A

CMV
EBV
VZV

153
Q

how do you test for type IV hypersensitivity?

A

candida extract skin test

154
Q

Does the absence of anti-dsDNA of anti-Smith rule out possibility of SLE?

A

NO–these are highly specific for ruling in

155
Q

recurrent Candida

PCP

A

No T cells

156
Q

Recurrent giardia infection

A

No B cells (no IgA)

157
Q

Recurrent candida and aspergillus

A

No granulocytes

158
Q

recurrent bacterial infections 6 months after birth

  • normal proB
  • low B cells
  • low Ig (all types)
A

Bruton’s X linked agammaglobulinemia

159
Q

Cause of bruton’ x linked agamma?

A

Defect in Bruton tyrosine kinase so NO B CELL MATURATION

160
Q

asymptomatic but recurrent sinopulmonary/GI infections. Also history of celiacs or other autoimmune.

A

Selective IgA deficiency.

161
Q

what do pts with selective IgA deficiency test false positive for?

A

beta HcG. cuz of heterophile antibody

162
Q

what is a heterophile antibody?

A

induced antibody that is characterized by broad reactivity with antibodies of other animal species

163
Q

pt in 20’s and 30s suddenly present with lymphoma and sinupulmonary infections. Normal B cell number but decreased plasma cells and immunoglobulin

A

CVID

164
Q

Cause of CVID

A

defect in B cell maturation

165
Q

pts with CVID increased risk of

A

autoimmune dz

166
Q

pt has tetany, recurrent viral/fungal infections

A

DiGeorge syndrome

167
Q

lab findings in Digeorge

A

absent thymic shadow

  • -low PTH
  • -low T cells
  • -low calcium
168
Q

cause of DiGeorge

A

22q11 =failure of 3rd and 4th branchial pouches to form

also cause of tetraology of fallot and persistent truncus arteriosus! cool!

169
Q

disseminated mycobacterial infections

A

IL-12 receptor deficiency

170
Q

lab findings in IL12 receptor deficiency

A

decreased IFN-y

171
Q

coarse facies
staphylococcal absecess
primary teeth retained
Eczema

A

Hyper IgE (Job’s syndrome)

172
Q

Cause of hyper IgE (Job’s)

A

Th1 cells fail to produce IFN-y

  • -neutrophils fail to go where they need to go
  • -will have lots of Th2 cells
173
Q

candida infections of skin and mucous membranes

A

Chronic mucocutaneous candidiasis

–caused by T cell dysfunction

174
Q

Failure to thrive, chronic diarrhea

–recurrent fungal, viral, bacterial infections

A

SCID

175
Q

XRay and lymph node biopsy findings in SCID

A 
Absence of thymic shadow
No germinal centers in lymph nodes
No B cells
--Decreased Tcell recombinant excision circles
--decreased T cells on flow cytometry
176
Q

cause of SCID

A
  1. Defective IL2 (most common)

2. Adenosine deaminase deficiency

177
Q

Ataxia, spider angiomas, and IgA deficiency

A

ataxia telangiectasia

178
Q

Cause of ataxia telangiectasia

A

Defects in ATM gene: codes for DNA repair enzymes

179
Q

Lab findings in Ataxia telangiectasia

A

Increased AFP

180
Q

Severe pyogenic infections early in life

A

Hyper IgM

181
Q

Cause of hyperIgM

A

defective CD40L cannot class switch

182
Q

thrombocytopenic purpura
infections
eczema

A

wiskott aldrich syndrome

183
Q

Cause of wiskott aldrich

A

WAS gene defective. T cells unable to reorganize actin cytoskeleton

184
Q

inheritance of wiskott aldrich

A

X linked

185
Q

Lab findings of wiskott aldrich

A

Increased IgE, IgA
Decreased IgM
Low platelets

186
Q

Recurrent bacterial infections, no pus, and delayed separation of umbilical cord

A

leukocyte adhesion deficiency

187
Q

Cause of Leukocyte adhesion deficiency

A

Defect in LFA-1 integrin (CD-18)

188
Q

lab findings in leukocyte adhesion deficiency

A

neutrophilia

189
Q

recurrent pyogenic infections by staph and strep

PARTIAL albinism and peripheral neuropathy

A

chediak higashi

190
Q

Cause of chediak higashi

A

Defect in lysosomal trafficking regulator gene (LYST). Microtubule dysfunction in phagosome-lysosome fusion

191
Q

inheritance of chediak higashi

A

Autosomal recessive

192
Q

giant granules in neutrophils

A

lab findings in chediak higashi

193
Q

abnormal dihydrorhodamine flow cytometry test

A

chronic granulomatous disease

194
Q

susceptibility to catalase positive organisms (S aureus, E coli, aspergillus)

A

chronic granulomatous disease

195
Q

cause: Chronic granulomatous disease

A

lack of NADPH oxidase. Cannot make reactive oxygen species in neutrophils

196
Q

Susceptible to BOTh catalase positive and negative orgs

A

myeloperoxidase deficiency. Cannot turn H2O2 into an O2 radical…EVEN though H2O2 is provided by catalase negative organisms!

197
Q

syngeneic graft

A

From identical twin

198
Q

acute rejection time frame

A

weeks

199
Q

chronic rejection time frame

A

months to years

200
Q

hyper acute rejection: type of hypersensitivity rxn?

A

Type II. preformed antibodies in transplant recipient attack donor cells (blood mismatch)

201
Q

occlusion of graft vessels causing ischemia and necrosis

A

hyperacute rejection

202
Q

vasculitis of graft vessels with dense intertitial lymphocytic infiltrate

A

acute rejection

203
Q

Fibrosis of graft tissue and blood vessels

A

chronic rejection.

204
Q

mechanism of acute rejection

A

Cell mediated

  • CTL react against foreign MHC
  • Reversible
205
Q

which rejection is NOT reversible?

A

chronic

206
Q

macropapular rash, jaundice, hepatosplenomegaly and diarrhea in a transplant pt

A

GVH disease

207
Q

which types of transplants most susceptible to GVH disease?

A

bone marrow and liver transplants (rich in lymphocytes)

208
Q

Mech: cyclosporin

A

blocks diff and activation of T cells

  • -inhibits calcineurin.
  • -No IL2 and IL2R
209
Q

tox of cyclosporine

A 
nephrotoxicity
hypertension
hyperlipidemia/glycemia
gingival hyperplasia
hirsutism
210
Q

Mech: tacrolimus

A

Binds FK binding protein, inhibiting calcineurin

211
Q

tox of tacrolimus (FK506)

A

same as cyclosporin, but NO gingival hyperplasia and NO hirsuitism

212
Q

Sirolimus (rapamycin) mechanism

A

Inhibits mTOR and T cell proliferation

213
Q

Use of sirolimus

A

tranplant and drug eluting stent

214
Q

toxicity: sirolimus

A

hyperlipidemia, thrombocytopenia, leukopenia

215
Q

mechanism: azathioprine

A

precursor of 6 MP

  • -interferes with synthesis of nucleic acids
  • -toxic to lymphocytes
216
Q

Use azathioprine

A

kidney transplant

–GN and hemolytic anemia

217
Q

Muromonab-CD3 (OKT3) mech

A

Binds CD3 and blocks T cell signal

218
Q

Tox of muromonab

A

cytokine release syndrome, hypersensitivity

219
Q

use: muromonab

A

kidney transplant

220
Q

Omalizumab

A

Anti-IgE for sever asthma

221
Q

aldesleukin

A

IL-2

222
Q

Use: aldesleukin

A

RCC

metastatic melanoma

223
Q

EPO

A

renal failure anemia

224
Q

filgrastim

A

GCSF

225
Q

sargramostim

A

GMCSF

226
Q

alpha IFN use:

A

Hep B, C
kaposi’s
leukemia
malignant melanoma

227
Q

B IFN

A

multiple sclerosis

228
Q

y interferon

A

chronic granulomatous disease

229
Q

Oprelvekin

A

thrombocytopenia

230
Q

Use: filgrastim/sargramostim:

A

Recovery of bone marrow

231
Q

trastuzumab

A

HER 2 antibody

232
Q

Describe the process of inflammatory leukocyte migration

A
  1. margination
  2. rolling: with sialyl acid binding to L, E or P selectin (induced by cytokines)
  3. activation of integrins
  4. MAC-1 and LFA-1 integrins bind ICAM-1 on leukocyte
  5. transmigration

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