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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. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Bind FcG for antibody dependent cellular cytotoxicity
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
neutrophilia!
B - T - and NK cells

2. What lymph node drains the sigmoid colon?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Inferior mesenteric
Antihistone
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

3. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgM and IgG
CRP - C3b - IgM
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

4. What are the autoantibodies for drug induced lupus?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antihistone
...

5. what secretes IL 4?
Basophils! THey want IG E class switch!
Immunosuppression after kidney transplantation
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Secretory component

6. What is the pathology of acute transplant rejection? is it reversible?
CD56
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

7. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

8. In thymic development - What is the positive selection? negative selections?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
The igA found in breast milk
When you select for which MHC it will have; take out the lymphs that self react
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

9. Which is the main antibody in the delayed or secondary response to an antigen?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antihistone
IgG
Anti smooth muscle

10. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Anti SS- A (anti RO) and Anti SS- B
Pernicious Anemia and Hashimotos
SP infections

11. What is the general structure of an Ab?
carboxy terminal
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
2 heavy chains and two light chains
acute phase reactants

12. Type Iv hypersensitivity is...
delayed!
A chemotactic factor for neutrophils
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
Rheumatic arthritis

13. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Anemias (esp due to renal failure)
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

14. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
...
By transcytosis
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

15. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgG
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
Wiskott Aldrich syndrome

16. What is chronic mucocutaneous candidiasis d/t?
IL 3; supports growth and differentiation of bone marrow stem cells
Interferon gamma; Th1
Axillary
T cell dysfunction

17. What is the mechanism for sirolimus? what else it known as?
Alternative splicing of mRNA
delayed!
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

18. which cells have more complete tolerance - B or T cells?
IL 4 - 5 - 10 - 6
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
T
Its main effect is a defect in Ab opsonization for killing

19. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
MS - hay fever - SLE - goodpastures
Cyclosporine - OKT3
Severe pyogenic infections early in life
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

20. What are the autoantibodies for autoimmune hepatitis?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti smooth muscle
IgG

21. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Superior mesenteric
Th cells fail to produce interferon gamma; a lot of IgE
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

22. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi

23. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Superficial inguinal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

24. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
If there is class switching and plasma cell production (that is when memory cells are produced)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

25. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Interferon gamma and IL 2
Celiac
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Paracortex

26. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Activates cytotoxic CD 8 T cells as second signal
CRP - C3b - IgM

27. What is the toxicity of azathioprine?
carboxy terminal
...
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
CRP - C3b - IgM

28. where are complements produced?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CRP - C3b - IgM
Axillary
Liver! (they are proteins circulating in the blood)

29. What is the white pulp of the spleen?
Previous transfusion; pregnant woman whose fetus had paternal antigens
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Receiving preformed Antibodies

30. What is recomb beta interferon used for?
MS
IgE; by activating eosinophils
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Th cells fail to produce interferon gamma; a lot of IgE

31. What is the presentation of hyperIgM syndrome?
IL 1 and IL 6
B - T - and NK cells
TGF beta and IL 10
Severe pyogenic infections early in life

32. What is recomb alpha interferon used for?
Recom IL 11; thrombocytopenia
Anemias (esp due to renal failure)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

33. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Not thymus - BM
Antibody mediated cytotoxicity; either complement dependent or complement independent
Histamine; post capillary venules - vasodilation
Anti glutamate carboxylase and anti insulin

34. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
T cell dysfunction
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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

35. What is passive immunity?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Receiving preformed Antibodies
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
active complement pathway

36. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anti alpha subunit 3 of collagen on type IV bm
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
opsonizes

37. What lymph node drains the testes?
A chemotactic factor for neutrophils
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Para aortic
Paracortex

38. Name 5 ways Antibody diversity is generated?
Anti topoisomerase
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
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

39. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antidesmoglein
Negative nitroblue tetrazolium reduction test
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

40. What does granzyme do? who secretes it?
IL 4 - 5 - 10 - 6
Its a serine protease that activates apoptosis; NK and CD8
Antimicrosomal and antithyroglobulin
Anti topoisomerase

41. What are the T cell functions?
IL 4 - 5 - 10 - 6
Carbohydrate
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
No because no peptide fragment!

42. Only the _______ contribute to the Fc region
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
heavy chains
TGF beta and IL 10
MHC class molecules bind to KIRS or CD94 to prevent killing

43. What is digoxin immune Fab used for?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
not Ab mediated
IgAs in mothers breast milk!
Antidote for digoxin intoxication

44. What type of side chains are found on Fc region of an antibody?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Carbohydrate
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

45. 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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

46. can igG cross the placenta?
Anti TSh receptor
Thrombocytopenia
Barrel hoop basement membrane fenestrations
Yes

47. Which helper T cells' development is induced by IL 4? IL 12?
heavy chains
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Th2; Th1

48. The idiotype; the Fc portion determines the...
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
isotype
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

49. 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
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
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
Para aortic

50. What are the autoantibodies for sjorgens syndrome?
acute phase reactants
Antibody mediated cytotoxicity; either complement dependent or complement independent
Fc
Anti SS- A (anti RO) and Anti SS- B

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