Flashcards in Immunology Deck (181)
Primary lymphoid organs (2):
Site of B cell localization in a lymph node:
Where the T cells in a lymph node are located:
(This is right next to the follicle)
Portion of a lymph node that becomes hugely enlarged in a robust cellular immune response:
Why do lymph nodes not enlarge in patients with DiGeorge?
They have no T cells. The paracortex, or T cell region, is what enlarges when a lymph node swells.
Where are the high endothelial venules of lymph nodes located?
T and B cells enter here
The primary lymph node drainage site for the upper limb and lateral breast:
The primary lymph node drainage site for the stomach:
The primary lymph node drainage site for the duodenum and jejunum:
Superior mesenteric nodes
The primary lymph node drainage site for the sigmoid colon:
Colic nodes, which drain to inferior mesenteric nodes
The primary lymph node drainage site for the rectum above the pectinate line:
Internal iliac nodes
The primary lymph node drainage site for the anal canal below the pectinate line:
Superficial inguinal nodes
The primary lymph node drainage site for the testes:
Superficial and deep para-aortic plexes
The primary lymph node drainage site for the scrotum:
Superficial inguinal nodes
What does the right lymphatic duct drain? What happens if you obstruct this duct or it gets damaged?
The right arm, chest, and right half of the head.
Damage -> non-pitting edema of RUE.
Where does the thoracic duct empty?
Jx of L subclavian and IJ
Three ways you can become asplenic:
Surgery (eg for spherocytosis)
Where are T cells in the spleen?
They live in the peri-arteriolar lymphatic sheath (PALS).
Remember, P for Paracortex (LN) and PALS (spleen).
Where are B cells found in the spleen?
In the follicles in the white pulp.
T/F: T cells are found in the red pulp of the spleen.
F. PALS is where they live, this is in the white pulp.
Post-splenectomy, 3 buzzwords:
Asplenia renders someone vulnerable to what organisms? Which do we have vaccines for?
Encapsulated ones. Even Some Killers Have Pretty Nice Capsules:
Strep pneumo *
H. influenzae *
Neisseria (mening. and gonococcal *)
From what embryonic structure does the thymus come? What other structure develops from this origin?
The 3rd branchial pouch. Inferior parathyroids develop with the thymus.
In the thymus, where do mature T cells live? What kind of selection are they undergoing here?
Mature T cells live in the Medulla of the thymus, here they are undergoing (-) selection (learning not to kill the host cells).
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.
The HLA subtypes associated with MHC I:
To what co-receptor does MHC I bind? MHC II?
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).
Which HLA subtypes are associated with MHC II?
Dr. is going to DQ to get a DrPepper.
Which MHC molecule needs to travel with b2 microglobulin to be displayed?
HLA associated with hemochromatosis:
HLA associated with the seronegative arthropathies:
Can you name 4 of these illnesses?
Ank. spondylitis, Reiters / reactive arthritis, IBD, psoriatic arthritis
HLA subtypes associated with celiac disease:
HLA-DQ2 / DQ8
HLA subtypes associated with MS, hay fever, SLE, and Goodpasture's
HLA associated with type 1 diabetes (2):
HLA-DR3 / DR4
HLA associated with pernicious anemia:
Two surface markers for NK cells:
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.
Cytokines that enhance NK cell activity:
NK cells secrete this cytokine to activate macrophages:
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.
Cell type that mediates hyperacute organ rejection:
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
This cytokine is secreted by TH2 cells to inhibit TH1 cell development:
These two cytokines are secreted by TH2 cells and stimulate B cells:
This interleukin drives TH1 development, where this interleukin drives TH2 development:
IL-12 drives TH1
IL-4 drives TH2
Which cell is the only cell that can activate a naive T cell?
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
The macrophage activating cytokine:
Two cytokines that inhibit TH1 cells:
(both from TH2 cells)
Cytokine TH1 cells secrete that inhibits TH2 cells:
Four buzz-words for cytotoxic T cell killing mechanisms:
Perforin (enters cell)
Granzyme (serine protease)
FAS ligand (+ FAS receptor on host cells)
Three things expressed on the surface of regulatory T cells?
Where does complement bind an Ab?
The Fc, CH2 region (just below the hinge).
Gene products responsible for VDJ recombination. What do these proteins recognize?
RAG1 & RAG2
Recognize recombination signal sequences = RSSs
There are two light chains in human Ab:
What is the normal ratio in humans?
Most abundant Ab:
Crosses the placenta:
Life expectancy of a maternal Ab in a baby:
Ab that is a dimer when secreted:
Ab that is found in colostrum:
Ab that mediates type I hypersensitivity:
Ab that fixes complement (2):
This Ab prevents attachment of bacteria to mucous membranes:
T/F: It fixes complement.
Two antibodies involved in the classic pathway of complement activation:
Triggers for each of the following complement pathways:
1. Classic = Ab mediated (IgG, IgM)
2. Leptin = mannose binding protein made by the liver
3. Alternative = molecules on the microbe
Complement protein for neutrophil chemotaxis:
Two other neutrophil chemotactic proteins:
IL-8, leukotriene B4
Complement proteins (2) responsible for anaphylaxis:
C3a, C5a for *A*naphylaxis
Complement proteins involved in forming the membrane attack complex:
Two complement proteins that help prevent complement from activating on self cells:
Decay-accelarating factor (DAF)
C1 esterase inhibitor = C1 esterase = C1 inhibitor
What is C1 esterase?
An inhibitor of the complement cascade, prevents host cells from being attacked by complement.
What does C1 esterase deficiency cause?
You do not give this medicine to patients with C1 esterase deficiency. Why?
C1 esterase def -> increased bradykinin, ACEi can also increase bradykinin
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.
C3 deficiency, in addition to being associated with infection, is also associated with a hypersensitivity reaction:
Type III (glomerulonephritis)
Deficiencies in C5-9 lead to susceptibility to infection with what kind of organisms?
Neisserii. We got both kinds.
What is the complement defeciency associated with paroxysmal nocturnal hemoglobinuria?
Deficiency in decay accelerating factor, an inhibitory protein.
DAF deficiency... what happens?
RBCs lyse (complement-mediated)
You get paroxysmal nocturnal hemoglobinuria.
These three acute phase reactants are secreted by macrophages:
This is the major chemotactic factor for neutrophils:
(C5a, leukotriene B)
Two interleukins that act as pyrogens:
The cytokine of septic shock:
What does IL-3 do?
Hot T-Bone stEAk:
IL-3 stimulates Bone marrow stem cells
IL-4 drives IgE production
Major T cell growth interleukin (all kinds of T cells):
What is the function of IFN-g?
Activates NK, TH1, macrophages.
Antiviral / anti-tumor.
What cell secretes these cytokines: IL-1, IL-6, IL-8, TNF-a:
What is the function of a and b interferons?
a- and b- inhibit viral protein synthesis.
IFN-g upregulates MHC I and II and antigen presentation.
Unique marker for T cells:
Unique marker for helper T cells:
Cytotoxic T cells:
Epsterin-Barr virus docks at this protein on the surface of B cells:
B at the Barr when you are 21.
Protein carried by all APCs:
What is special about CD56?
It is the unique marker for NK cells.
This molecule binds the Fc of IgG:
Four exposures you might want to consider passively immunizing someone for:
If you want to confer passive immunity to someone, how often would you need to dose them?
Roughly monthly. t1/2 =~3w.
These vaccines are live-attenuated:
Oral polio = sabin
These two vaccines are egg based, contraindicated in people with severe allergies:
(MMR technically, though not a problem in administration)
Which of the polio vaccines is live?
Oral is live (Sabin)
Injectable is inactivated (Salk)
Live or killed? Cholera:
Live or killed? Yellow fever:
Live or killed? Sabin polio:
Live or killed? Hep A vaccine:
Live or killed? Rabies vaccine:
Live or killed? MMR:
The three hypersensitivity reactions that are mediated by antibodies?
The one mediated by cells?
I-III are Ab mediated
IV is cell-mediated
Hypersensitivity associated with IgE:
Hypersensitivity associated with IgM / IgG vs. cells:
Hypersensitivity associated with delayed response:
Hypersensitivity associated with immune complex formation and neutrophil activation:
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.
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.
The 3 things stuck together in type III hypersensitivity:
PSGN is an example of this kind of hypersensitivity:
Type III (Ab vs. antigen depositing in tissues)
Rheumatic fever is an example of this kind of hypersensitivity:
Type II (Ab vs. self)
Allergic and atopic disorders fall into the category of this kind of hypersensitivity:
Multiple sclerosis is an example of this kind of hypersensitivity:
The PPD test for TB is an example of this kind of hypersensitivity:
Pernicious anemia is an example of this kind of hypersensitivity:
Type II (Ab vs host protein)
Goodpasture syndrome is an example of this kind of hypersensitivity:
Type II (anti-GBM Ab, NOT immune complex deposition)
SLE and RA are both an example of this kind of hypersensitivity:
Type III, oddly.
Acute hemolytic transfusion reaction... what type of hypersensitivity am I?
Can be intravascular (ABO incompatible) or extravascular (host Ab vs. foreign antigen on donor cell).
What kinds of infections would someone who had no granulocytes be vulnerable to (4)?
Someone with no B cells would be particularly vulnerable to this viral infection:
Anti-dsDNA is most commonly seen in this autoimmune disorder:
SLE (more specific for renal involvement)
Anti-Smith Ab are seen in:
Anti-histone Ab are most commonly seen in this autoimmune disorder:
You measure a positive RF for someone you suspect has RA. What is your confirmatory test?
Ab associated with sceroderma:
Antimitochondrial Ab are found in this disease:
Primary biliary cirrhosis
Ab for Goodpasture syndrome:
Ab for Hashimoto (2):
Anti-desmoglein Ab are most commonly seen in this autoimmune disorder:
You suspect Sjogren syndrome. Order these two Ab titers especially:
Anti-smooth muscle Ab are seen with this disease:
c-ANCA Ab are seen in this illness:
Granulomatosis with polyangiitis (Wegener's granulomatosis)
p-ANCA Ab are seen in these disorders (2):
These two Ab may mark Type 1 DM:
Anti-islet cell Ab
Anti-glutamate decarboxylase Ab
You suspect autoimmune hepatitis. What Ab titer do you order?
Anti-smooth muscle Ab
A deficiency of this cell type would leave someone particularly prone to GI giardiasis. Why?
There is no IgA to guard the gut
The three main X-linked immunodeficiencies you deemed it prudent to study:
Immunodeficiency linked with a defective tyrosine kinase:
Bruton's X-linked agammaglobulinemia
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.
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
Most common primary immunodeficiency:
Selective IgA deficiency
What happens if you give IgA containing blood products to someone with selective IgA deficiency?
Immunodeficiency assoc. with 22q11:
IL-12 receptor deficiency leads to a decrease in this type of cell response:
Immunodeficiency associated with tetany:
Suspect this deficiency in a child with disseminated mycobacterial infections:
IL-12 deficiency --> absence of TH1 response
T cell disorder in which primary teeth are retained:
Job's syndrome (hyper-IgE)
What cytokine is deficient in Job's syndrome?
High IgE, eosinophilia, and a failure of neutrophils to deal with business:
Job's syndrome (hyper-IgE)
Cold staph abscesses and eczema:
Defective NADPH oxidase:
Treatment for CGD:
Truncal eczema is associated with this immune deficiency disease:
Immunodeficiency with high IgA, low IgM, high IgE:
This immune deficiency results from a defective adenosine deaminase enzyme:
Absence of thymic shadow, T cells, and germinal centers is associated with which immune deficiency? What are the two most common causal genetic defects?
IL-2 receptor malformed
Adenosine deaminase deficiency
Tyrosine kinase defect is associated with which immune deficiency disorder?
Severe pyogenic infections early in life in the presence of both B and T cells are associated with which immune deficiency?
Immune deficiency with elevated AFP:
Immune deficiency in which the only intact part of the immune system is NK cells:
Mode of inheritence for CGD:
Immune deficiency disease where you would see neutrophils filled with giant granules:
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.
Albinism and problems with infections, what disease am I?
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.
Immune deficiency in which you would be susceptible to infection by S. aureus, E. coli, Aspergillus, Klebsiella, and Candida:
You have no respiratory burst, can still make H2O2, but can't kill catalase (+) organisms.
Immune disease associated with the triad of thrombocytopenia, eczema, and infections:
What's the other one where you are likely to see eczema?
Job's, Hyper IgE
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:
I am an immunodeficiency associated with neutrophilia. What protein is defective?
Leukocyte adhesion deficiency.
CD18 = LFA-1 integrin defect.
In a child with delayed separation of the umbilical cord, suspect:
Leukocyte adhesion deficiency
Langerhans cell histiocytosis -- dendritic cell would have this characteristic inclusion:
Birbeck granule, shaped like a tennis racket
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)
Which cytokines inhibit T cells?
IFN-g inhibits TH2 cells
IL-10 inhibits TH1 cells
Macrophages produce three important acute-phase cytokines:
What is a degmacyte?
A bite cell, an RBC a macrophage has chomped to get at something inside it (ex denatured Hb).