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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.
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 is the toxicity of azathioprine?
IgA
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
...
False! B cell class switching requires a second signal

2. What are C1 - C2 - C3 - C4 important for?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Influenza; antigenic shift; antigenic drift
Viral neutralization of igM and IgG!
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

3. What is a factor that is a predictor for a bad transplantation?
Acts as second signal on B cells to induce class switching to IgE and IgG
Its main effect is a defect in Ab opsonization for killing
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

4. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
In the germinal center of secondary follicles (In the paler center)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

5. Which diseases are associated with DR5?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti IF
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Pernicious Anemia and Hashimotos

6. Which disease is associated with HLA A3?
Anti viral and anti tumor
Hemochromatosis
cannot cross placenta
Pernicious Anemia and Hashimotos

7. Which is the main antibody that provides passive immunity to infants?
Anti TSh receptor
MS
IgG
The igA found in breast milk

8. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Antidote for digoxin intoxication
Kill them because they have CD16 on them that recognize the FcG portion
Daclizumab; prevent ACUTE rejection of renal transplant
CRP - C3b - IgM

9. hat is the presentation of Jobs syndrome or Hyper IgE?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
A j chain

10. What lymph node drains the testes?
A j chain
By transcytosis
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Para aortic

11. What type of fenestrations are found in the red pulp of the spleen?
Antibody mediated cytotoxicity; either complement dependent or complement independent
IL 4 - 5 - 10 - 6
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Barrel hoop basement membrane fenestrations

12. Which antibodies can be multimeric?
IgM and IgA
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
C5a

13. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Cyclosporine - OKT3
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
neutrophilia!
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

14. What is the most common selective Ig deficiency? What is the presentation?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Its main effect is a defect in Ab opsonization for killing
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
IL 3; supports growth and differentiation of bone marrow stem cells

15. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
By transcytosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

16. What is the main function of IL 12? other than macrophages who else can release IL 12?
Basophils! THey want IG E class switch!
Recom IL 11; thrombocytopenia
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

17. What is the pathology seen in chronic transplant rejection?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
CD21 on B cells (although there is T cell lymphocytosis in EBV)
If there is class switching and plasma cell production (that is when memory cells are produced)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

18. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Inferior mesenteric
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

19. can igG cross the placenta?
Receiving preformed Antibodies
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Yes

20. What are the symptoms of serum sickness?
heavy chains
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Edema and necrosis in that region

21. What is serum sickness? give an example.
isotype
Local infection/inflammation; infection of the ln itself; metastasis
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

22. 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
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
Internal iliac
IL 5

23. ________ regulate the cell mediated response.
Humoral
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

24. What is the clinical use for sirolimus? what should you combine it with?
mesenchymal
Wiskott Aldrich syndrome
Internal iliac
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

25. What are the autoantibodies for myasthenia gravis?
Anti viral and anti tumor
Popliteal
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti Ach receptor

26. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Anti TSh receptor
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
All MHC 1/CD8
IgA

27. What does Interferon alpha and beta do? how?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
carboxy terminal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Rheumatic arthritis

28. What are the T cell functions?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Para aortic
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti Ach receptor

29. What cytokines are released by Th1 cells?
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Interferon gamma and IL 2
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

30. Other than stimulating fever - what else does IL 6 do?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Its main effect is a defect in Ab opsonization for killing
Stimulate the liver to release acute phase reactants

31. describe the classic complement pathway.
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
Antidesmoglein
IL 5
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

32. when can graft versus host disease? What is the result?
Cells that stil have weird parts of their membrane that macrophages usually bite off
RNA segment reassortment
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
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)

33. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
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

34. How fast does it occur?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
The patient could become cyanotic in the OR!
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

35. What is muromonab - CD3 (OKT3)
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
Wiskott Aldrich syndrome
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A - B - C; all the D's

36. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Tetanus - Botulinum - HBV - Rabies
Carbohydrate
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

37. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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

38. For which toxins are preformed antibodies (passive) given?
T
Basophils! THey want IG E class switch!
Tetanus - Botulinum - HBV - Rabies
Recom IL 11; thrombocytopenia

39. What does interferon gamma do? What two type of cells does it attack mostly?
Rheumatic arthritis
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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

40. which cytokine inhibits TH2 cells? secreted by who?
opsonizes
Interferon gamma; Th1
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
Delayed type hypersensitivity

41. What is the receptor for EBV? On what cells is that located?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
MHC I - CD16 - CD56
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Receiving preformed Antibodies

42. where are complements produced?
Kill them because they have CD16 on them that recognize the FcG portion
Viral neutralization of igM and IgG!
pale central germinal centers
Liver! (they are proteins circulating in the blood)

43. How does igA cross the epithelium?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
By transcytosis
Secretory component
...

44. which interleukin receptor is required for NK development? activation?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 15; IL 12 - interferon Beta and interferon alpha

45. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
encapsulated
IgE
DM type I and RA

46. How is the thymus organized? what happens in each section?
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
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
not Ab mediated
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

47. The alternative pathway is the only constutively...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
active complement pathway
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

48. What do mature naive B lymphocytes express?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgM and IgD
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

49. 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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

50. What lymph node drains the scrotum?
Superficial inguinal
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
Para aortic
except hyperacute