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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 are the autoantibodies for drug induced lupus?
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
SP infections
Antihistone
DM type I

2. which antibody activate mast cells - basophils - and eosinophils?
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
Popliteal
Anti TSh receptor
IgE

3. Which antibody mediates immunity to worms? how?
...
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgE; by activating eosinophils

4. What is the pathogenesis of a hypersensitivity reaction?
IL 5
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
Secretory component
TLR ad nuclear receptors

5. Describe the Mannose Lectin pathway
IgM and 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
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

6. What lymph node drains the testes?
Para aortic
Antidesmoglein
The patient could become cyanotic in the OR!
Severe pyogenic infections early in life

7. can igG cross the placenta?
Yes
Activates cytotoxic CD 8 T cells as second signal
Viral neutralization of igM and IgG!
IgG

8. What is the pathology seen in chronic transplant rejection?
delayed!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Internal iliac

9. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti Ach receptor

10. What is the pathogenesis of a candida skin test?
Receiving preformed Antibodies
Hereditary angioedema; PNH
Delayed type hypersensitivity
Influenza; antigenic shift; antigenic drift

11. What are the autoantibodies for goodpastures syndrome?
IgE
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti alpha subunit 3 of collagen on type IV bm
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

12. What are the autoantibodies for pernicious anemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
cannot cross placenta
secondary
Anti IF

13. in which immunodef order do you see a lot of pus? no pus?
NK cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
In the germinal center of secondary follicles (In the paler center)
Axillary

14. Name the three opsonins
CRP - C3b - IgM
CD56
Anti Jo -1
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

15. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
T cell dysfunction
IgE; by activating eosinophils
IL 4 - 5 - 10 - 6

16. Which disease is associated with B8?
Antimicrosomal and antithyroglobulin
Macrophages - Dendritic cells - B cells
TGF beta and IL 10
Graves

17. IgM can fix complement but...
Anti alpha subunit 3 of collagen on type IV bm
cannot cross placenta
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
Cross link

18. What is the clinical use for azathioprine?
...
Superior mesenteric
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

19. What is passive immunity?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Delayed type hypersensitivity
Receiving preformed Antibodies
Type IV

20. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
active complement pathway
Stimulate the liver to release acute phase reactants
False! B cell class switching requires a second signal

21. Which cytokines do Th2 release and For what?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

22. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

23. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
C5a
opsonizes
Inferior mesenteric
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

24. What are the PALS?
Axillary
Superficial inguinal
TLR ad nuclear receptors
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

25. which antibodies prevent antigens from binding mucosal surfaces?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
pale central germinal centers
IgA

26. How does the alternative pathway lead to MAC activation?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Severe pyogenic infections early in life
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

27. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
not Ab mediated
...
Its main effect is a defect in Ab opsonization for killing

28. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Previous transfusion; pregnant woman whose fetus had paternal antigens
Negative selection
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

29. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
Anemias (esp due to renal failure)
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

30. What cytokines are released by Th1 cells?
Viral neutralization of igM and IgG!
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Interferon gamma and IL 2
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

31. What is Aldesleukin? What is it used for
encapsulated
Hemochromatosis
A recomb cytokine of IL 2; RCC and metastatic melanoma
Tetanus - Botulinum - HBV - Rabies

32. The lymphocytes are ________ origin
mesenchymal
Anti mitochondrial
T cell activation; no with CD 4 or CD 8
CD21 on B cells (although there is T cell lymphocytosis in EBV)

33. when can graft versus host disease? What is the result?
IL 5
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
Type IV
Lymphocytes

34. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antidote for digoxin intoxication
...
B - T - and NK cells

35. what prevents NK cells from killing normal cells if their default is to kill?
Paracortex
MHC class molecules bind to KIRS or CD94 to prevent killing
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

36. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Antihistone
...
IgE; by activating eosinophils
TNF alpha and IL1

37. The pathogenesis of contact dermatitis is ________ hypersensitivity
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
T cell dysfunction
type four
Inferior mesenteric

38. To what portion of the Antibody do the complements bind?
Fc
The patient could become cyanotic in the OR!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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

39. 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
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
Superior mesenteric
IgG

40. what results in symptoms of shock in an acute hemolytic transfusion reaction?
IL 4 - 5 - 10 - 6
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Popliteal

41. Which HLA's are included in MHC I? MHC II?

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42. What is the common variable immunodeficiency ? How is it different from Brutons?
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
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti IF

43. How is sirolimus different from tacrolimus?
IgE
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Its main effect is a defect in Ab opsonization for killing
Anti mitochondrial

44. which B and T cell disorder presents with specifically low IgM?
Negative nitroblue tetrazolium reduction test
Wiskott Aldrich syndrome
T cell precursor
Rheumatic arthritis

45. What are the cell surface proteins for Macrophages? which two are for opsonins?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Histamine; post capillary venules - vasodilation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Antihistone

46. describe the pathogenesis of delayed type IV hypersensitivity
Anti glutamate carboxylase and anti insulin
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Hemochromatosis
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

47. The two heavy chains of an antibody contribute to the...
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
C5a
Carbohydrate
Fab portion

48. What are the autoantibodies for pemphigus bulgaris?
carboxy terminal
Antidesmoglein
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
dimer

49. How does igA cross the epithelium?
By transcytosis
Anemias (esp due to renal failure)
TLR ad nuclear receptors
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

50. Only the _______ contribute to the Fc region
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
heavy chains
A j chain
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)