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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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. which cells have more complete tolerance - B or T cells?
T
Anti U1 RNP (ribonucleoprotein)
Immunosuppression after kidney transplantation
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

2. Which is the main antibody that provides passive immunity to infants?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
IgG
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

3. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Sinusitis - otitis media - pneumonia
...
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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

4. What are the two signals to kill for NK cells?
MHC I; from RER with help of the B2 microglobulin
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MS
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

5. What is the presentation of common variable immunodef? and What are the labs?
DM type I and RA
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Antimicrosomal and antithyroglobulin
isotype

6. What are the autoantibodies for other vasculitides?
Popliteal
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

7. What is the treatment of acute transplant rejection?
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Cyclosporine - OKT3
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

8. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Edema and necrosis in that region
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
RNA segment reassortment
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

9. What is the main function of IL 12? other than macrophages who else can release IL 12?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Tetanus - Botulinum - HBV - Rabies
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
TGF beta and IL 10

10. What does IL 5 do?
encapsulated
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Acts as second signal on B cells to induce class switching to IgE and IgG
Kill them because they have CD16 on them that recognize the FcG portion

11. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
SP infections
Anti topoisomerase
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
A - B - C; all the D's

12. For which toxins are preformed antibodies (passive) given?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Tetanus - Botulinum - HBV - Rabies
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

13. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Immunosuppression after kidney transplantation
MHC I - CD16 - CD56
Macrophages - Dendritic cells - B cells
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)

14. Describe the Mannose Lectin pathway
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Anti topoisomerase
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

15. What is a type I hypersensitivity reaction? What is atopic?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
IgM
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

16. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Complement activation (active in both)
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
Antimicrosomal and antithyroglobulin

17. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Para aortic
Fc
B - T - and NK cells

18. What lymph node drains the breast?
Axillary
pale central germinal centers
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
Popliteal

19. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Wiskott Aldrich syndrome
IgG
acute phase reactants

20. What is the pathogenesis of a candida skin test?
Acts as second signal on B cells to induce class switching to IgE and IgG
Delayed type hypersensitivity
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CRP - C3b - IgM

21. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
No because no peptide fragment!
neutrophilia!
Previous transfusion; pregnant woman whose fetus had paternal antigens

22. So antibodies are the effectors for the humoral response. List some of their functions.
Receiving preformed Antibodies
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Axillary
IgM and IgG

23. Type IV hypersensitivity is i...
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
not Ab mediated
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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

24. where are complements produced?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Liver! (they are proteins circulating in the blood)
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
Antidesmoglein

25. What are the PALS?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs

26. In thymic development - What is the positive selection? negative selections?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
No because no peptide fragment!
When you select for which MHC it will have; take out the lymphs that self react
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

27. What is the pathology seen in chronic transplant rejection?
neutrophilia!
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Macrophages - Dendritic cells - B cells
Its main effect is a defect in Ab opsonization for killing

28. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Pernicious Anemia and Hashimotos
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
except hyperacute

29. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Graves
mesenchymal
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

30. How is the antigen loaded onto a MHC II?
S. aureus - E. Coli - aspergillus
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

31. What is muromonab - CD3 (OKT3)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

32. is IgM an opsonizer?
T cell dysfunction
Negative!
Axillary
Histamine; post capillary venules - vasodilation

33. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TGF beta and IL 10
IgM and IgG

34. are Th cells involved in trapping of antigens of endotoxin/LPS?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
No because no peptide fragment!
Secretory component
False! B cell class switching requires a second signal

35. IgE has the ___________ in the serum
secondary
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
lowest concentration

36. The alternative pathway is the only constutively...
Sinusitis - otitis media - pneumonia
active complement pathway
IgE
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

37. What lymph node drains the anal canal (below the pectinate line)?
pathogenesis
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Superior mesenteric
Superficial inguinal

38. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Its a serine protease that activates apoptosis; NK and CD8
Negative!
Anti U1 RNP (ribonucleoprotein)

39. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
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
Superficial inguinal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

40. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
active complement pathway
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
2 heavy chains and two light chains

41. which interleukin receptor is required for NK development? activation?
S. aureus - E. Coli - aspergillus
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)
IL 15; IL 12 - interferon Beta and interferon alpha
The patient could become cyanotic in the OR!

42. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Anemias (esp due to renal failure)
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
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

43. T/F B cells do not require a second signal
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
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Hemochromatosis
False! B cell class switching requires a second signal

44. where do NK cells develop?
Superficial inguinal
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
TLR ad nuclear receptors
Not thymus - BM

45. What are the autoantibodies for pernicious anemia?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti IF
Edema and necrosis in that region
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs

46. What are the two signals required for Th1 cells? what happens after then activated?
Not thymus - BM
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

47. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
acute phase reactants
Activates Th1 helper cells; Macrophages

48. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
IL 3; supports growth and differentiation of bone marrow stem cells
type four
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

49. which antibody activate mast cells - basophils - and eosinophils?
IgE
delayed!
Acts as second signal on B cells to induce class switching to IgE and IgG
Interferon gamma and IL 2

50. What is the most common example of passive immunity?
IgAs in mothers breast milk!
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Axillary
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids