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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 part of the lymph node specifically expands during a cellular immune response? when would this occur?
MS - hay fever - SLE - goodpastures
Chronic granulomatous disease
Increases expression of MHC I and MHC II and also activates NK cells
Paracortex; viral infection

2. What cytokines to Th2 secrete?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
TNF alpha and IL1
delayed!
IL 4 - 5 - 10 - 6

3. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antihistone

4. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
T cell dysfunction
Antimicrosomal and antithyroglobulin
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

5. What is the defect in hyper IgM syndrome? What are the lab results?
Immunoflourescent staining of tissue biopsies
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Chronic granulomatous disease
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

6. The idiotype; the Fc portion determines the...
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
secondary
isotype
Inferior mesenteric

7. Monomer in circulation - ___ when secreted
Glycoproteins; HLA
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
dimer
IgG

8. What does IL 2 do?
TLR ad nuclear receptors
T cell dysfunction
Activates cytotoxic CD 8 T cells as second signal
DM type I

9. are Th cells involved in trapping of antigens of endotoxin/LPS?
Cells that stil have weird parts of their membrane that macrophages usually bite off
No because no peptide fragment!
Not thymus - BM
Hemochromatosis

10. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
TGF beta and IL 10
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Histamine; post capillary venules - vasodilation

11. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
pathogenesis
Superficial inguinal
Rheumatic arthritis

12. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Popliteal
Yes

13. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Rheumatic arthritis
Sinusitis - otitis media - pneumonia

14. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
Anti Jo -1
Cross link
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

15. Which disease is associated with DR7?
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
Severe pyogenic infections early in life
Steroid responsive nephrotic syndrome
T

16. where do NK cells develop?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
When you select for which MHC it will have; take out the lymphs that self react
Not thymus - BM
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

17. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
A - B - C; all the D's
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
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

18. What are the autoantibodies for polymyositis and dermatomyositis?
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
Superficial inguinal
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti Jo -1

19. what secretes IL 4?
isotype
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Stimulate the liver to release acute phase reactants
Basophils! THey want IG E class switch!

20. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
A - B - C; all the D's
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

21. What lymph node drains the anal canal (below the pectinate line)?
Tetanus - Botulinum - HBV - Rabies
Anti TSh receptor
Anti mitochondrial
Superficial inguinal

22. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Acts as second signal on B cells to induce class switching to IgE and IgG
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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

23. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
type four
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

24. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Viral neutralization of igM and IgG!
IgG
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
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

25. what cell surface marker is used for NK cells as it is unique to them?
2 heavy chains and two light chains
Fab portion
Antimicrosomal and antithyroglobulin
CD56

26. Other than stimulating fever - what else does IL 6 do?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Stimulate the liver to release acute phase reactants
Liver! (they are proteins circulating in the blood)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

27. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
...
RNA segment reassortment

28. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
Popliteal
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

29. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
IgE
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

30. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
acute phase reactants
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
B - T - and NK cells
IgAs in mothers breast milk!

31. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
except hyperacute

32. How does complement link innate and adaptive?
Steroid responsive nephrotic syndrome
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

33. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Delayed type hypersensitivity
Interferon gamma; Th1
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

34. A lymph node is a ________ lymphoid organ.
Stimulate the liver to release acute phase reactants
Macrophages - Dendritic cells - B cells
Not thymus - BM
secondary

35. is IgM an opsonizer?
Negative!
Anti alpha subunit 3 of collagen on type IV bm
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
heavy chains

36. What lymph node drains the sigmoid colon?
When you select for which MHC it will have; take out the lymphs that self react
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Inferior mesenteric
Cytokine IL 10 secreted by Th2

37. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
heavy chains

38. What is the most common example of passive immunity?
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
...
IgAs in mothers breast milk!
Bind FcG for antibody dependent cellular cytotoxicity

39. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
IL 15; IL 12 - interferon Beta and interferon alpha
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Influenza; antigenic shift; antigenic drift
Remove encapsulated bacateria

40. Which helper T cells' development is induced by IL 4? IL 12?
Axillary
Antimicrosomal and antithyroglobulin
Th2; Th1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

41. What is filgrastim and sargramostim? and What is it used for?
NK cells
Complement activation (active in both)
CD56
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

42. The secondary follicles have __________; primary follicles are dense
B - T - and NK cells
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
pale central germinal centers
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

43. Which disease is associated with DR3?
Anti IF
By transcytosis
DM type I
A recomb cytokine of IL 2; RCC and metastatic melanoma

44. What bugs can actually infect the lymph node itself?
pathogenesis
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

45. Which disease is associated withB B27?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Rheumatic arthritis
T cell dysfunction
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

46. What are the main symptoms of T cell immunodeficiencies?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti U1 RNP (ribonucleoprotein)

47. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
B - T - and NK cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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!
Its main effect is a defect in Ab opsonization for killing

48. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
...
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
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
Antimicrosomal and antithyroglobulin

49. How is i Th1 helper cell inhibited?
IgG
Negative nitroblue tetrazolium reduction test
Cytokine IL 10 secreted by Th2
IgAs in mothers breast milk!

50. What are the autoantibodies for type I diabetes mellitus?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti glutamate carboxylase and anti insulin
Tetanus - Botulinum - HBV - Rabies