Immunology Flashcards
(181 cards)
1
Q
Primary lymphoid organs (2):
A
Thymus
Bone marrow
2
Q
Site of B cell localization in a lymph node:
A
Follicle
3
Q
Where the T cells in a lymph node are located:
A
Paracortex
This is right next to the follicle
4
Q
Portion of a lymph node that becomes hugely enlarged in a robust cellular immune response:
A
Paracortex
5
Q
Why do lymph nodes not enlarge in patients with DiGeorge?
A
They have no T cells. The paracortex, or T cell region, is what enlarges when a lymph node swells.
6
Q
Where are the high endothelial venules of lymph nodes located?
A
Paracortex
T and B cells enter here
7
Q
The primary lymph node drainage site for the upper limb and lateral breast:
A
Axillary
8
Q
The primary lymph node drainage site for the stomach:
A
Celiac nodes
9
Q
The primary lymph node drainage site for the duodenum and jejunum:
A
Superior mesenteric nodes
10
Q
The primary lymph node drainage site for the sigmoid colon:
A
Colic nodes, which drain to inferior mesenteric nodes
11
Q
The primary lymph node drainage site for the rectum above the pectinate line:
A
Internal iliac nodes
12
Q
The primary lymph node drainage site for the anal canal below the pectinate line:
A
Superficial inguinal nodes
13
Q
The primary lymph node drainage site for the testes:
A
Superficial and deep para-aortic plexes
14
Q
The primary lymph node drainage site for the scrotum:
A
Superficial inguinal nodes
15
Q
What does the right lymphatic duct drain? What happens if you obstruct this duct or it gets damaged?
A
The right arm, chest, and right half of the head.
Damage -> non-pitting edema of RUE.
16
Q
Where does the thoracic duct empty?
A
Jx of L subclavian and IJ
17
Q
Three ways you can become asplenic:
A
Sickle cell
Trauma
Surgery (eg for spherocytosis)
18
Q
Where are T cells in the spleen?
A
They live in the peri-arteriolar lymphatic sheath (PALS).
Remember, P for Paracortex (LN) and PALS (spleen).
19
Q
Where are B cells found in the spleen?
A
In the follicles in the white pulp.
20
Q
T/F: T cells are found in the red pulp of the spleen.
A
F. PALS is where they live, this is in the white pulp.
21
Q
Post-splenectomy, 3 buzzwords:
A
Howell-Jolly bodies
Target cells
Thrombocytosis
22
Q
Asplenia renders someone vulnerable to what organisms? Which do we have vaccines for?
A
Encapsulated ones. Even Some Killers Have Pretty Nice Capsules: E. coli Strep pneumo * Klebsiella H. influenzae * Pseudomonas Neisseria (mening. and gonococcal *) Cryptococcus
23
Q
From what embryonic structure does the thymus come? What other structure develops from this origin?
A
The 3rd branchial pouch. Inferior parathyroids develop with the thymus.
24
Q
In the thymus, where do mature T cells live? What kind of selection are they undergoing here?
A
Mature T cells live in the Medulla of the thymus, here they are undergoing (-) selection (learning not to kill the host cells).
25
In the thymus, where do immature T cells live? What kind of selection are they going through here?
Immature T cells live in the cortex.
Mature live in the Medulla.
They are undergoing (+) selection and learning to talk MHC.
26
The HLA subtypes associated with MHC I:
HLA-A
HLA-B
HLA-C
27
To what co-receptor does MHC I bind? MHC II?
CD8
| CD4
28
Which cells express MHC I?
| Which cells express MHC II?
MHC I is on the surface of all nucleated cells.
| MHC II is only on APCs (macs, B cells, dendritic cells).
29
Which HLA subtypes are associated with MHC II?
Dr. is going to DQ to get a DrPepper.
HLA-DR
HLA-DQ
HLA-DP
30
Which MHC molecule needs to travel with b2 microglobulin to be displayed?
MHC I
31
HLA associated with hemochromatosis:
HLA-A3
32
HLA associated with the seronegative arthropathies:
| Can you name 4 of these illnesses?
HLA-B27
| Ank. spondylitis, Reiters / reactive arthritis, IBD, psoriatic arthritis
33
HLA subtypes associated with celiac disease:
HLA-DQ2 / DQ8
34
HLA subtypes associated with MS, hay fever, SLE, and Goodpasture's
HLA-DR2
35
HLA associated with type 1 diabetes (2):
HLA-DR3 / DR4
36
HLA associated with pernicious anemia:
HLA-DR5
37
Two surface markers for NK cells:
CD-16
| CD-56
38
T/F: NK cells require T cell help to induce apoptosis of infected / cancerous cells:
F. They use perforin and granzymes on their own, respond to coded antigen and absence of MHC I.
39
Cytokines that enhance NK cell activity:
IL-2
IL-12
IFN-b
IFN-a
40
NK cells secrete this cytokine to activate macrophages:
IFN-g
41
What does CD-16 do and what cell types carry it?
Killers have it (macs, neut, monos, NK).
| It binds the constant region of Ab and targets the Ab bearing cell for destruction.
42
Cell type that mediates hyperacute organ rejection:
B cells
43
TH1 cells secrete two main stimulatory cytokines. What do they do?
IFN-g calls out to macrophages
IFN-g also inhibits other T cells from going down the TH2 path
IL-2 stimulates T cells, NK cells
44
This cytokine is secreted by TH2 cells to inhibit TH1 cell development:
IL-10
45
These two cytokines are secreted by TH2 cells and stimulate B cells:
IL-4
| IL-5
46
This interleukin drives TH1 development, where this interleukin drives TH2 development:
IL-12 drives TH1
| IL-4 drives TH2
47
Which cell is the only cell that can activate a naive T cell?
Dendritic cell
48
Three APCs:
Dendritic cell
Macrophage
B cell
49
A naive T cell requires MHC + antigen + appropriate co-stimulation. What are these costimulatory molecules? A B cell requires a different pair of costimulatory moleucles, what are they?
CD28 on the T cell
CD80 = CD86 = B7 on the dendritic cell
CD40 on the B cell
CD40 ligand on the T cell
50
The macrophage activating cytokine:
IFN-g
51
Two cytokines that inhibit TH1 cells:
IL-4
IL-10
(both from TH2 cells)
52
Cytokine TH1 cells secrete that inhibits TH2 cells:
IFN-g
53
Four buzz-words for cytotoxic T cell killing mechanisms:
Perforin (enters cell)
Granzyme (serine protease)
Granulysin
FAS ligand (+ FAS receptor on host cells)
54
Three things expressed on the surface of regulatory T cells?
CD3
CD4
CD25
55
Where does complement bind an Ab?
The Fc, CH2 region (just below the hinge).
56
Gene products responsible for VDJ recombination. What do these proteins recognize?
RAG1 & RAG2
| Recognize recombination signal sequences = RSSs
57
There are two light chains in human Ab:
| What is the normal ratio in humans?
kappa
lambda
2K:1L
58
Most abundant Ab:
IgG
59
Crosses the placenta:
IgG
60
Life expectancy of a maternal Ab in a baby:
~21d
61
Ab that is a dimer when secreted:
IgA
62
Ab that is found in colostrum:
IgA
63
Ab that mediates type I hypersensitivity:
IgE
64
Ab that fixes complement (2):
IgG, IgM
65
This Ab prevents attachment of bacteria to mucous membranes:
| T/F: It fixes complement.
IgA
| F. No.
66
Two antibodies involved in the classic pathway of complement activation:
IgG
| IgM
67
Triggers for each of the following complement pathways:
1. Classic
2. Lectin
3. Alternative
1. Classic = Ab mediated (IgG, IgM)
2. Leptin = mannose binding protein made by the liver
3. Alternative = molecules on the microbe
68
Complement protein for neutrophil chemotaxis:
| Two other neutrophil chemotactic proteins:
C5a
| IL-8, leukotriene B4
69
Complement proteins (2) responsible for anaphylaxis:
C3a, C5a for *A*naphylaxis
70
Complement proteins involved in forming the membrane attack complex:
C5b-9
71
Two complement proteins that help prevent complement from activating on self cells:
Decay-accelarating factor (DAF)
| C1 esterase inhibitor = C1 esterase = C1 inhibitor
72
What is C1 esterase?
An inhibitor of the complement cascade, prevents host cells from being attacked by complement.
73
What does C1 esterase deficiency cause?
Hereditary angioedema.
74
You do not give this medicine to patients with C1 esterase deficiency. Why?
ACEi
| C1 esterase def -> increased bradykinin, ACEi can also increase bradykinin
75
What happens to people who have a C3 deficiency?
They cannot coat bacteria with C3. They end up with severe recurrent pyogenic sinus / resp tract infections.
76
C3 deficiency, in addition to being associated with infection, is also associated with a hypersensitivity reaction:
Type III (glomerulonephritis)
77
Deficiencies in C5-9 lead to susceptibility to infection with what kind of organisms?
Neisserii. We got both kinds.
78
What is the complement defeciency associated with paroxysmal nocturnal hemoglobinuria?
Deficiency in decay accelerating factor, an inhibitory protein.
79
DAF deficiency... what happens?
```
RBCs lyse (complement-mediated)
You get paroxysmal nocturnal hemoglobinuria.
```
80
These three acute phase reactants are secreted by macrophages:
IL-1
IL-6
TNF-a
81
This is the major chemotactic factor for neutrophils:
IL-8
| C5a, leukotriene B
82
Two interleukins that act as pyrogens:
IL-1
| IL-6
83
The cytokine of septic shock:
TNF-a
84
What does IL-3 do?
| IL-4?
Hot T-Bone stEAk:
IL-3 stimulates Bone marrow stem cells
IL-4 drives IgE production
85
Major T cell growth interleukin (all kinds of T cells):
IL-2
86
What is the function of IFN-g?
Activates NK, TH1, macrophages.
Suppresses TH2.
Antiviral / anti-tumor.
87
What cell secretes these cytokines: IL-1, IL-6, IL-8, TNF-a:
Macrophages
88
What is the function of a and b interferons?
| g interferons?
a- and b- inhibit viral protein synthesis.
| IFN-g upregulates MHC I and II and antigen presentation.
89
Unique marker for T cells:
CD3
90
Unique marker for helper T cells:
| Cytotoxic T cells:
CD4
| CD8
91
Epsterin-Barr virus docks at this protein on the surface of B cells:
CD21
| B at the Barr when you are 21.
92
Protein carried by all APCs:
CD40
93
What is special about CD56?
It is the unique marker for NK cells.
94
This molecule binds the Fc of IgG:
CD16
95
Four exposures you might want to consider passively immunizing someone for:
Tetanus
Botulism
HBV
Rabies
96
If you want to confer passive immunity to someone, how often would you need to dose them?
Roughly monthly. t1/2 =~3w.
97
These vaccines are live-attenuated:
```
MMR
Oral polio = sabin
Varicella
Yellow fever
Intranasal flu
```
98
These two vaccines are egg based, contraindicated in people with severe allergies:
Flu
Yellow fever
(MMR technically, though not a problem in administration)
99
Which of the polio vaccines is live?
Oral is live (Sabin)
| Injectable is inactivated (Salk)
100
Live or killed? Cholera:
Killed
101
Live or killed? Yellow fever:
Live
102
Live or killed? Sabin polio:
= Oral
| Live
103
Live or killed? Hep A vaccine:
Killed
104
Live or killed? Rabies vaccine:
Killed
105
Live or killed? MMR:
Killed
106
The three hypersensitivity reactions that are mediated by antibodies?
The one mediated by cells?
I-III are Ab mediated
| IV is cell-mediated
107
Hypersensitivity associated with IgE:
Type I
108
Hypersensitivity associated with IgM / IgG vs. cells:
Type II
109
Hypersensitivity associated with delayed response:
Type IV
110
Hypersensitivity associated with immune complex formation and neutrophil activation:
Type III
111
What causes the Arthus reaction? What kind of hypersensitivity is this?
Antigen-Ab complexes in the skin get attacked by neutrophils. This is Type III hypersensitivity.
112
What is serum sickness?
Give someone foreign proteins.
Ab vs foreign proteins are made by host.
These Ab form complexes that deposit on membranes, inflammation causes damage.
This is Type III hypersensitivity.
113
The 3 things stuck together in type III hypersensitivity:
Antigen
Ab
Complement
114
PSGN is an example of this kind of hypersensitivity:
Type III (Ab vs. antigen depositing in tissues)
115
Rheumatic fever is an example of this kind of hypersensitivity:
Type II (Ab vs. self)
116
Allergic and atopic disorders fall into the category of this kind of hypersensitivity:
Type I
117
Multiple sclerosis is an example of this kind of hypersensitivity:
Type IV
118
The PPD test for TB is an example of this kind of hypersensitivity:
Type IV
119
Pernicious anemia is an example of this kind of hypersensitivity:
Type II (Ab vs host protein)
120
Goodpasture syndrome is an example of this kind of hypersensitivity:
Type II (anti-GBM Ab, NOT immune complex deposition)
121
SLE and RA are both an example of this kind of hypersensitivity:
Type III, oddly.
122
Acute hemolytic transfusion reaction... what type of hypersensitivity am I?
Type II.
| Can be intravascular (ABO incompatible) or extravascular (host Ab vs. foreign antigen on donor cell).
123
What kinds of infections would someone who had no granulocytes be vulnerable to (4)?
Staph
Brukholderia cepacia
Serratia
Nocardia
124
Someone with no B cells would be particularly vulnerable to this viral infection:
Enteroviral encephalitis
125
Anti-dsDNA is most commonly seen in this autoimmune disorder:
SLE (more specific for renal involvement)
126
Anti-Smith Ab are seen in:
SLE
127
Anti-histone Ab are most commonly seen in this autoimmune disorder:
DIL
128
You measure a positive RF for someone you suspect has RA. What is your confirmatory test?
Anti-CCP Ab
129
Ab associated with sceroderma:
Anti-centromere (CREST)
| Anti-Scl-70 (diffuse)
130
Antimitochondrial Ab are found in this disease:
Primary biliary cirrhosis
131
Anti-endomysial Ab:
Celiac disease
132
Ab for Goodpasture syndrome:
Anti-BM
133
Ab for Hashimoto (2):
Anti-thyroglobulin
| Anti-microsomal
134
Anti-desmoglein Ab are most commonly seen in this autoimmune disorder:
Pemphigus vulgaris
135
You suspect Sjogren syndrome. Order these two Ab titers especially:
Anti-Ro (SSA)
| Anti-La (SSB)
136
Anti-smooth muscle Ab are seen with this disease:
Autoimmune hepatitis
137
c-ANCA Ab are seen in this illness:
Granulomatosis with polyangiitis (Wegener's granulomatosis)
138
p-ANCA Ab are seen in these disorders (2):
Microscopic polyangiitis
| Churg-Strauss syndrome
139
These two Ab may mark Type 1 DM:
Anti-islet cell Ab
| Anti-glutamate decarboxylase Ab
140
You suspect autoimmune hepatitis. What Ab titer do you order?
Anti-smooth muscle Ab
141
A deficiency of this cell type would leave someone particularly prone to GI giardiasis. Why?
B cells
| There is no IgA to guard the gut
142
The three main X-linked immunodeficiencies you deemed it prudent to study:
Wiskott-Aldrich
Bruton's agammaglobulinemia
CGD
Hyper-IgM
143
Immunodeficiency linked with a defective tyrosine kinase:
Bruton's X-linked agammaglobulinemia
144
Clinical presentation of a patient with Bruton's X-linked agammaglobulinemia:
6 months into life, child with recurrent bacterial infections. Low B cell count, low Ig of all types.
145
Disorder in which there is no B cell maturation:
| Disorder in which B cell maturation becomes defective:
Bruton's X-linked agammaglobulinemia
| Common variable immunodeficiency
146
Most common primary immunodeficiency:
Selective IgA deficiency
147
What happens if you give IgA containing blood products to someone with selective IgA deficiency?
Anaphylaxis
148
Immunodeficiency assoc. with 22q11:
DiGeorge
149
IL-12 receptor deficiency leads to a decrease in this type of cell response:
TH1
150
Immunodeficiency associated with tetany:
DiGeorge
151
Suspect this deficiency in a child with disseminated mycobacterial infections:
IL-12 deficiency --> absence of TH1 response
152
T cell disorder in which primary teeth are retained:
Job's syndrome (hyper-IgE)
153
What cytokine is deficient in Job's syndrome?
IFN-g
154
High IgE, eosinophilia, and a failure of neutrophils to deal with business:
Job's syndrome (hyper-IgE)
155
Cold staph abscesses and eczema:
Job's syndrome
156
Defective NADPH oxidase:
CGD
157
Treatment for CGD:
IFN-g
| TMP-SMX prophylaxis
158
Truncal eczema is associated with this immune deficiency disease:
Wiskott-Aldrich.
159
Immunodeficiency with high IgA, low IgM, high IgE:
Wiskott-Aldrich
160
This immune deficiency results from a defective adenosine deaminase enzyme:
SCID
161
Absence of thymic shadow, T cells, and germinal centers is associated with which immune deficiency? What are the two most common causal genetic defects?
SCID
IL-2 receptor malformed
Adenosine deaminase deficiency
162
Tyrosine kinase defect is associated with which immune deficiency disorder?
Bruton's agammaglobulinemia
163
Severe pyogenic infections early in life in the presence of both B and T cells are associated with which immune deficiency?
Hyper IgM
164
Immune deficiency with elevated AFP:
Ataxia-telangiectasia.
165
Immune deficiency in which the only intact part of the immune system is NK cells:
SCID
166
Mode of inheritence for CGD:
X-linked
167
Immune deficiency disease where you would see neutrophils filled with giant granules:
Chediak-Higashi
168
Cerebellar defects and immune deficiency, what disease am I? What would you see on labs?
Ataxia-telangiectasia. See high AFP, low IgA and T lymphs.
169
Albinism and problems with infections, what disease am I?
Chediak-Higashi
170
I am a child with recurrent staph and strep infections and peripheral neuropathy. What is my gene defect? Mode of inheritence for my disorder?
LYST = problem with phagosome / lysosome fusion. Autosomal recessive. This is Chediak-Higashi.
171
Immune deficiency in which you would be susceptible to infection by S. aureus, E. coli, Aspergillus, Klebsiella, and Candida:
CGD.
| You have no respiratory burst, can still make H2O2, but can't kill catalase (+) organisms.
172
Immune disease associated with the triad of thrombocytopenia, eczema, and infections:
What's the other one where you are likely to see eczema?
Wiskott-Aldrich
WAITER mnemonic
Job's, Hyper IgE
173
You see spider angiomas in a 5-year-old child with poor visual smooth pursuit. Before you put them in front of an X-ray film, stop! Suspect this immunodeficiency:
Ataxia telangiectasia.
174
I am an immunodeficiency associated with neutrophilia. What protein is defective?
Leukocyte adhesion deficiency.
| CD18 = LFA-1 integrin defect.
175
In a child with delayed separation of the umbilical cord, suspect:
Leukocyte adhesion deficiency
176
Langerhans cell histiocytosis -- dendritic cell would have this characteristic inclusion:
Birbeck granule, shaped like a tennis racket
177
What molecules are on the surface of a dendritic cell that is prepared to present antigen?
MHC I / II
CD80 / 86
CD40 (expressed by all APC)
178
Which cytokines inhibit T cells?
IFN-g inhibits TH2 cells
| IL-10 inhibits TH1 cells
179
Macrophages produce three important acute-phase cytokines:
IL-1
IL-6
TNF-a
180
What is a degmacyte?
A bite cell, an RBC a macrophage has chomped to get at something inside it (ex denatured Hb).
181
Why are people with asplenia prone to thrombocytosis?
Spleen sequesters platelets.
| Platelets with no home are in the circulation -> thrombocytosis.
