USMLE Step 1 Immunology

Instructions:

• Answer 50 questions in 15 minutes.
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• Match each statement with the correct term.
• Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. What are the two signals required for Th1 cells? what happens after then activated?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
T cell activation; no with CD 4 or CD 8
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Increases expression of MHC I and MHC II and also activates NK cells


2. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
MHC I - CD16 - CD56
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)


3. give an example of how influenza does a major antigenic shift.
Antibody mediated cytotoxicity; either complement dependent or complement independent
...
RNA segment reassortment
The igA found in breast milk


4. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Macrophages - Dendritic cells - B cells


5. What is epo used for?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
DM type I
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anemias (esp due to renal failure)


6. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
cannot cross placenta
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Severe pyogenic infections early in life


7. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
B - T - and NK cells
MHC class molecules bind to KIRS or CD94 to prevent killing


8. How is sirolimus different from tacrolimus?
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Secretory component


9. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IgA
Bind FcG for antibody dependent cellular cytotoxicity
IgG


10. In general What are T cells good for?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgM
Anti Ach receptor
Anti viral and anti tumor


11. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
IL 4
IgAs in mothers breast milk!


12. What lymph node drains the sigmoid colon?
Inferior mesenteric
Edema and necrosis in that region
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs


13. Monomer in circulation - ___ when secreted
except hyperacute
lowest concentration
dimer
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal


14. which antibody activate mast cells - basophils - and eosinophils?
mesenchymal
Sinusitis - otitis media - pneumonia
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
IgE


15. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Axillary
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles


16. describe the pathogenesis of delayed type IV hypersensitivity
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Tetanus - Botulinum - HBV - Rabies


17. What is an example of a parasite showing antigenic variation?
TGF beta and IL 10
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
T cell dysfunction


18. What are the mediators that mast cells release?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
T
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)


19. What are some catalase positive organisms?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
S. aureus - E. Coli - aspergillus


20. Which helper T cells' development is induced by IL 4? IL 12?
Increases expression of MHC I and MHC II and also activates NK cells
Th2; Th1
CRP - C3b - IgM
Lymphocytes


21. which cells have more complete tolerance - B or T cells?
...
T
Yes
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur


22. IgG...
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Superior mesenteric
Thrombocytopenia
opsonizes


23. How do you test for type III hypersensitivity?
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Immunoflourescent staining of tissue biopsies
Immunosuppression after kidney transplantation
Severe pyogenic infections early in life


24. What lymph node drains the testes?
MHC class molecules bind to KIRS or CD94 to prevent killing
Para aortic
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
acute phase reactants


25. what bacteria are a splenectomy patient most susceptible to? why?
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IL 3; supports growth and differentiation of bone marrow stem cells
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs


26. Which type of selection of thymic development provides central tolerance?
Negative selection
Negative nitroblue tetrazolium reduction test
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
IgM and IgD


27. __________ are a part of the innate system.
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Influenza; antigenic shift; antigenic drift
NK cells
except hyperacute


28. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
B - T - and NK cells
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton


29. What is the mechanism for sirolimus? what else it known as?
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
S. aureus - E. Coli - aspergillus
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig


30. What can cause a lymph node enlargement?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
NK cells
RNA segment reassortment
Local infection/inflammation; infection of the ln itself; metastasis


31. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Alternative splicing of mRNA
Anti TSh receptor
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)


32. What are the autoantibodies for wegeners granulomatosis?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Steroid responsive nephrotic syndrome
A - B - C; all the D's
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic


33. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
C5a
Hemochromatosis
Alternative splicing of mRNA
neutrophilia!


34. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
neutrophilia!
IgM and IgA


35. The MALT/GALT are not...
encapsulated
Histamine; post capillary venules - vasodilation
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Remove encapsulated bacateria


36. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
B - T - and NK cells
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
NK cells


37. Which diseases are associated with DR4?
IgG
DM type I and RA
Superior mesenteric
IgM and IgD


38. Only the _______ contribute to the Fc region
dimer
heavy chains
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Pernicious Anemia and Hashimotos


39. What is hereditary angioedema? What are the C3 levels?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC I - CD16 - CD56
Popliteal
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx


40. which antibodies can bind complement?
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Immunosuppression after kidney transplantation
delayed!
IgM and IgG


41. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II


42. What lymph node drains the upper limb?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Axillary
IgA
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)


43. What happens in a secondary follicle?
carboxy terminal
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Superficial inguinal
CD56


44. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
CRP - C3b - IgM
Its a serine protease that activates apoptosis; NK and CD8


45. What is the clinical use for azathioprine?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
not Ab mediated
...


46. Type Iv hypersensitivity is...
False! B cell class switching requires a second signal
delayed!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Previous transfusion; pregnant woman whose fetus had paternal antigens


47. Describe complement dependent Type II hypersensitivity. Give an example.
Alternative splicing of mRNA
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Complement activation (active in both)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated


48. How does complement link innate and adaptive?
False! B cell class switching requires a second signal
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Sinusitis - otitis media - pneumonia


49. Which is the main antibody that provides passive immunity to infants?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgG
mesenchymal
...


50. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
CD56
A - B - C; all the D's
Influenza; antigenic shift; antigenic drift
...