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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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 happens in a deficiency of C1 esterase inhibitor? DAF?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anti Ach receptor
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Hereditary angioedema; PNH

2. is IgM an opsonizer?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Negative!
Alternative splicing of mRNA

3. What lymph node drains the anal canal (below the pectinate line)?
DM type I
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Superficial inguinal
Anti viral and anti tumor

4. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Interferon gamma; Th1
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
Activate macrophages
IgG

5. Complements are...
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
acute phase reactants
B - T - and NK cells
When you select for which MHC it will have; take out the lymphs that self react

6. What is the main cytokine released by T cells? What does it do
Interferon gamma and IL 2
Not thymus - BM
IL 3; supports growth and differentiation of bone marrow stem cells
Antimicrosomal and antithyroglobulin

7. What do mature naive B lymphocytes express?
Anti Ach receptor
IgM and IgD
Type IV
Viral neutralization of igM and IgG!

8. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Kill them because they have CD16 on them that recognize the FcG portion
Anemias (esp due to renal failure)
Glycoproteins; HLA
IL 4

9. What is the main cytokine that activates eosinophils?
2 heavy chains and two light chains
IL 5
TGF beta and IL 10
Activates cytotoxic CD 8 T cells as second signal

10. What is the general structure of an Ab?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
2 heavy chains and two light chains

11. What are four results of a splenectomy?
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)
Edema and necrosis in that region
MHC I - CD16 - CD56
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

12. What type of side chains are found on Fc region of an antibody?
IL 15; IL 12 - interferon Beta and interferon alpha
B - T - and NK cells
C5a
Carbohydrate

13. What is the toxicity of azathioprine?
...
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Chronic granulomatous disease
TNF alpha and IL1

14. What are the autoantibodies for primary biliary cirrhosis?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti mitochondrial
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

15. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Fc
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Superficial inguinal

16. What lymph node drains the lateral side of the dorsum of the foot?
lowest concentration
MHC II - B7
Popliteal
IL 15; IL 12 - interferon Beta and interferon alpha

17. What is the most common selective Ig deficiency? What is the presentation?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgG
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Carbohydrate

18. The pathogenesis of contact dermatitis is ________ hypersensitivity
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Local infection/inflammation; infection of the ln itself; metastasis
type four

19. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IL 4 - 5 - 10 - 6
IL 3; supports growth and differentiation of bone marrow stem cells
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

20. How does complement link innate and adaptive?
except hyperacute
Axillary
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

21. IgG...
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
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
opsonizes
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

22. 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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
dimer

23. What are the cell surface proteins for Macrophages? which two are for opsonins?
TNF alpha and IL1
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

24. How does igA cross the epithelium?
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
Secretory component
Inferior mesenteric
By transcytosis

25. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
Anti TSh receptor
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

26. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Th2; Th1
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

27. What is the main function of interferons?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
S. aureus - E. Coli - aspergillus
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

28. What is the toxicity of muromonab?
Anti TSh receptor
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Negative selection

29. What is an example of a parasite showing antigenic variation?
not Ab mediated
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

30. What can cause a lymph node enlargement?
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
Local infection/inflammation; infection of the ln itself; metastasis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti Jo -1

31. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Influenza; antigenic shift; antigenic drift
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
opsonizes

32. What lymph node drains the sigmoid colon?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Inferior mesenteric
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
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

33. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Para aortic
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
Increases expression of MHC I and MHC II and also activates NK cells

34. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
IL 1 and IL 6
Not thymus - BM
Increases expression of MHC I and MHC II and also activates NK cells

35. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Liver! (they are proteins circulating in the blood)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Type IV
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

36. Which disease is associated withB B27?
Superficial inguinal
Tetanus - Botulinum - HBV - Rabies
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

37. What does interferon gamma do to be antiviral?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Increases expression of MHC I and MHC II and also activates NK cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

38. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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)
Activates cytotoxic CD 8 T cells as second signal
Barrel hoop basement membrane fenestrations

39. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Severe pyogenic infections early in life
Edema and necrosis in that region
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

40. What does it mean if there are igM in the serum at birth?
Hereditary angioedema; PNH
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)
IgM and IgG

41. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
T cell precursor
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgM and IgG

42. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
except hyperacute
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

43. What are the autoantibodies for hashimotos?
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Antimicrosomal and antithyroglobulin
...

44. What is the mechanism for sirolimus? what else it known as?
The patient could become cyanotic in the OR!
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
Anti Jo -1
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

45. give an example of how influenza does a major antigenic shift.
Edema and necrosis in that region
Hereditary angioedema; PNH
Anti alpha subunit 3 of collagen on type IV bm
RNA segment reassortment

46. From where do cytokines come from?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
dimer
Lymphocytes
Cells that stil have weird parts of their membrane that macrophages usually bite off

47. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

48. What are the autoantibodies for drug induced lupus?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
Antihistone
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

49. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
neutrophilia!
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
pale central germinal centers

50. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy