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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 end result of complement activation? what bugs are this important for? through what pathway and why?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
IL 4 - 5 - 10 - 6

2. The secondary follicles have __________; primary follicles are dense
Glycoproteins; HLA
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
Viral neutralization of igM and IgG!
pale central germinal centers

3. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
neutrophilia!
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

4. What does it mean if there are igM in the serum at birth?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Recom IL 11; thrombocytopenia
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Liver! (they are proteins circulating in the blood)

5. What is the toxicity of azathioprine?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
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
...

6. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Anti glutamate carboxylase and anti insulin
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

7. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
TLR ad nuclear receptors
pentamer
except hyperacute
Activates Th1 helper cells; Macrophages

8. 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
Anti Ach receptor
Delayed type hypersensitivity
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

9. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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

10. what secretes IL 4?
Basophils! THey want IG E class switch!
not Ab mediated
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti TSh receptor

11. What lymph node drains the testes?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Para aortic
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
dimer

12. Monomer in circulation - ___ when secreted
dimer
Secretory component
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

13. when can graft versus host disease? What is the result?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

14. Which disease is associated with HLA A3?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
mesenchymal
Hemochromatosis
Anti topoisomerase

15. Which disease is associated withB B27?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Glycoproteins; HLA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

16. where do somatic hypermutation and class switching occur?
Negative selection
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Chronic granulomatous disease
In the germinal center of secondary follicles (In the paler center)

17. What are the three types of APCs?
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Macrophages - Dendritic cells - B cells

18. what cytokine does basophils secrete?
IL 4
type four
Cyclosporine - OKT3
IgM and IgA

19. Complements are...
acute phase reactants
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
B - T - and NK cells
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

20. What are the PALS?
Humoral
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 5
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

21. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
...
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
MHC I - CD16 - CD56

22. What is the marginal zone of the spleen? what happens there?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
NK cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

23. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Lymphocytes

24. What are C1 - C2 - C3 - C4 important for?
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
Complement activation (active in both)
Delayed type hypersensitivity
Viral neutralization of igM and IgG!

25. What is the presentation of Brutons agammaglobulinemia?
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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

26. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
Lymphocytes
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

27. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgE; by activating eosinophils
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
heavy chains

28. What is chronic mucocutaneous candidiasis d/t?
IgE
IgM and IgA
Activates Th1 helper cells; Macrophages
T cell dysfunction

29. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
delayed!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

30. Name two endogenous pyrogens
Local infection/inflammation; infection of the ln itself; metastasis
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 1 and IL 6
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

31. What are the autoantibodies for myasthenia gravis?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti Ach receptor
cannot cross placenta
IgA

32. What is the presentation of hyperIgM syndrome?
IL 15; IL 12 - interferon Beta and interferon alpha
Severe pyogenic infections early in life
DM type I
Activate macrophages

33. What is colostrum?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
MHC I; from RER with help of the B2 microglobulin
The igA found in breast milk
All MHC 1/CD8

34. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
T

35. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

36. What is the presentation of common variable immunodef? and What are the labs?
Superficial inguinal
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IL 5

37. What is the toxicity of muromonab?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
not Ab mediated

38. what happens in a deficiency of C1 esterase inhibitor? DAF?
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
IL 15; IL 12 - interferon Beta and interferon alpha
Axillary
Hereditary angioedema; PNH

39. Which disease is associated with B8?
IgE; by activating eosinophils
Graves
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
T cell precursor

40. In general What are T cells good for?
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti viral and anti tumor
IgM and IgG

41. Type IV hypersensitivity is i...
Sinusitis - otitis media - pneumonia
not Ab mediated
TNF alpha and IL1
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

42. what prevents NK cells from killing normal cells if their default is to kill?
...
MHC class molecules bind to KIRS or CD94 to prevent killing
A - B - C; all the D's
IgE

43. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
Glycoproteins; HLA
Antibody mediated cytotoxicity; either complement dependent or complement independent
Not thymus - BM

44. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anemias (esp due to renal failure)
A j chain
T cell precursor

45. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

46. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Carbohydrate
Basophils! THey want IG E class switch!
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

47. What lymph node drains the upper limb?
Axillary
Severe pyogenic infections early in life
The igA found in breast milk
RNA segment reassortment

48. What are the autoantibodies for type I diabetes mellitus?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
By transcytosis
Anti glutamate carboxylase and anti insulin
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

49. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Local infection/inflammation; infection of the ln itself; metastasis
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)
A chemotactic factor for neutrophils
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a

50. What do mature naive B lymphocytes express?
NK cells
Carbohydrate
Active; passive - fast but short half life (3 weeks!)
IgM and IgD