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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 recomb beta interferon used for?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
MS

2. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Previous transfusion; pregnant woman whose fetus had paternal antigens

3. What type of side chains are found on Fc region of an antibody?
If there is class switching and plasma cell production (that is when memory cells are produced)
encapsulated
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Carbohydrate

4. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Hemochromatosis
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
mesenchymal

5. other than C3a - what other complement acts as an anaphyloxin?
Cyclosporine - OKT3
C5a
active complement pathway
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

6. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Delayed type hypersensitivity
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IL 4
MHC II - B7

7. What is the pathogenesis of a hypersensitivity reaction?
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Humoral
secondary

8. What are the autoantibodies for primary biliary cirrhosis?
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
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!
Anti mitochondrial
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

9. What is serum sickness? give an example.
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Antidote for digoxin intoxication
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

10. What is a type I hypersensitivity reaction? What is atopic?
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

11. Which is the main antibody that provides passive immunity to infants?
NK cells
Cyclosporine - OKT3
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgG

12. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
isotype
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
Daclizumab; prevent ACUTE rejection of renal transplant

13. which antibodies can bind complement?
Axillary
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MS
IgM and IgG

14. Which disease is associated with DR3?
DM type I
Fc
Receiving preformed Antibodies
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

15. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Superficial inguinal
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

16. What is passive immunity?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Receiving preformed Antibodies
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

17. What is epo used for?
Anemias (esp due to renal failure)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Fc
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

18. What are the autoantibodies for drug induced lupus?
Antihistone
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A - B - C; all the D's
A recomb cytokine of IL 2; RCC and metastatic melanoma

19. What is the white pulp of the spleen?
TLR ad nuclear receptors
By transcytosis
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

20. What lymph node drains the sigmoid colon?
Inferior mesenteric
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Negative selection
By transcytosis

21. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
...
Sinusitis - otitis media - pneumonia

22. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Barrel hoop basement membrane fenestrations
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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

23. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Steroid responsive nephrotic syndrome

24. 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
CD56
CRP - C3b - IgM
Activates cytotoxic CD 8 T cells as second signal

25. What are the autoantibodies for goodpastures syndrome?
Para aortic
Anti alpha subunit 3 of collagen on type IV bm
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

26. describe the classic complement pathway.
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Its main effect is a defect in Ab opsonization for killing
Graves

27. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
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
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

28. What are the main Cell surface proteins on T cells?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
mesenchymal

29. What is the mechanism for sirolimus? what else it known as?
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

30. How fast does it occur?
Negative!
The patient could become cyanotic in the OR!
Local infection/inflammation; infection of the ln itself; metastasis
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

31. What is the main cytokine released by T cells? What does it do
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 3; supports growth and differentiation of bone marrow stem cells
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

32. What is thrombopoietin used for?
Alternative splicing of mRNA
Thrombocytopenia
MS
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

33. The MALT/GALT are not...
Its main effect is a defect in Ab opsonization for killing
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
encapsulated
RNA segment reassortment

34. What are the labs in brutons agammaglobulinemia?
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

35. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgM and IgA
Antidote for digoxin intoxication
IL 4 - 5 - 10 - 6

36. How does igA cross the epithelium?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti TSh receptor
By transcytosis
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

37. What is the main function of interferons?
Histamine; post capillary venules - vasodilation
IgE
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Increases expression of MHC I and MHC II and also activates NK cells

38. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
carboxy terminal
Superficial inguinal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

39. give an example of how influenza does a major antigenic shift.
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IgG
RNA segment reassortment

40. What lymph node drains the testes?
Para aortic
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgM and IgD
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

41. Which are the only two antiinflammatory cytokines?
Local infection/inflammation; infection of the ln itself; metastasis
not Ab mediated
TGF beta and IL 10
Receiving preformed Antibodies

42. What is digoxin immune Fab used for?
Internal iliac
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Superficial inguinal
Antidote for digoxin intoxication

43. What is the toxicity of muromonab?
Axillary
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

44. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
2 heavy chains and two light chains
Anemias (esp due to renal failure)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

45. The two heavy chains of an antibody contribute to the...
Fab portion
RNA segment reassortment
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

46. The ______ in the BM are DN - the DP are in the cortex of thymus
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
T cell precursor
Acts as second signal on B cells to induce class switching to IgE and IgG
not Ab mediated

47. are Th cells involved in trapping of antigens of endotoxin/LPS?
IL 4 - 5 - 10 - 6
Celiac
No because no peptide fragment!
Pernicious Anemia and Hashimotos

48. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Internal iliac
Stimulate the liver to release acute phase reactants
IgG

49. From where do cytokines come from?
Rheumatic arthritis
Negative!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Lymphocytes

50. Leukocyte adhesion defect presents with...
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
pentamer
neutrophilia!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction