Test your basic knowledge |

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 are some sinopulmonary infections?
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Sinusitis - otitis media - pneumonia
...

2. What is the presentation of Brutons agammaglobulinemia?
Anti viral and anti tumor
Anti SS- A (anti RO) and Anti SS- B
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cytokine IL 10 secreted by Th2

3. What is filgrastim and sargramostim? and What is it used for?
isotype
Cells that stil have weird parts of their membrane that macrophages usually bite off
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti Jo -1

4. which interleukin receptor is required for NK development? activation?
carboxy terminal
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 15; IL 12 - interferon Beta and interferon alpha
Antimicrosomal and antithyroglobulin

5. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Local infection/inflammation; infection of the ln itself; metastasis
Liver! (they are proteins circulating in the blood)
Graves

6. What is a type I hypersensitivity reaction? What is atopic?
neutrophilia!
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

7. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Immunoflourescent staining of tissue biopsies
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!

8. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Humoral
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

9. 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?
Immunoflourescent staining of tissue biopsies
TGF beta and IL 10
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

10. What are C1 - C2 - C3 - C4 important for?
T cell precursor
not Ab mediated
Negative nitroblue tetrazolium reduction test
Viral neutralization of igM and IgG!

11. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

12. What are four results of a splenectomy?
Anti TSh receptor
Sinusitis - otitis media - pneumonia
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgE; by activating eosinophils

13. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Th cells fail to produce interferon gamma; a lot of IgE
pathogenesis

14. What is the defect in hyper IgM syndrome? What are the lab results?
Anti U1 RNP (ribonucleoprotein)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Tetanus - Botulinum - HBV - Rabies
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

15. 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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cyclosporine - OKT3
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

16. What is the marginal zone of the spleen? what happens there?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Pernicious Anemia and Hashimotos
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

17. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Yes
Barrel hoop basement membrane fenestrations
Cytokine IL 10 secreted by Th2

18. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
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

19. What does IL 4 do?
NK cells
Para aortic
Acts as second signal on B cells to induce class switching to IgE and IgG
IgM and IgD

20. What are the autoantibodies for other vasculitides?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
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

21. What are superantigens? give two examples.
MS - hay fever - SLE - goodpastures
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Axillary
Negative nitroblue tetrazolium reduction test

22. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
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!
MHC II - B7
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

23. What is the main function of IL 8?
A chemotactic factor for neutrophils
Previous transfusion; pregnant woman whose fetus had paternal antigens
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
MHC class molecules bind to KIRS or CD94 to prevent killing

24. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anti SS- A (anti RO) and Anti SS- B
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

25. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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!
Interferon gamma; Th1
IL 3; supports growth and differentiation of bone marrow stem cells
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

26. What are the autoantibodies for pemphigus bulgaris?
Anti IF
TNF alpha and IL1
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antidesmoglein

27. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Immunosuppression after kidney transplantation

28. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

29. which cells have more complete tolerance - B or T cells?
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Barrel hoop basement membrane fenestrations
T

30. Describe the capsular structure of a lymph node; What are the functions of the LN?
In the germinal center of secondary follicles (In the paler center)
Anti alpha subunit 3 of collagen on type IV bm
SP infections
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

31. A lymph node is a ________ lymphoid organ.
NK cells
MHC II - B7
secondary
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

32. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
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
Pernicious Anemia and Hashimotos
False! B cell class switching requires a second signal

33. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Severe pyogenic infections early in life
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
False! B cell class switching requires a second signal

34. 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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Superior mesenteric
Activates cytotoxic CD 8 T cells as second signal

35. 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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Th cells fail to produce interferon gamma; a lot of IgE
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

36. What are target cells?
Delayed type hypersensitivity
Popliteal
Cells that stil have weird parts of their membrane that macrophages usually bite off
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

37. What are the autoantibodies for systemic sclerosis?
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
Anti alpha subunit 3 of collagen on type IV bm
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti topoisomerase

38. How does igA cross the epithelium?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Sinusitis - otitis media - pneumonia
Anti smooth muscle
By transcytosis

39. which of the hypersensitivity reactions is not Ab mediated?
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Type IV
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

40. is IgM an opsonizer?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Negative!
Fc

41. what ensure that a memory response is generated?
TNF alpha and IL1
If there is class switching and plasma cell production (that is when memory cells are produced)
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

42. What are the PALS?
Activate macrophages
Histamine; post capillary venules - vasodilation
MS
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

43. How is sirolimus different from tacrolimus?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Graves
Antimicrosomal and antithyroglobulin

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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Not thymus - BM

45. What is chronic mucocutaneous candidiasis d/t?
IgG
T cell dysfunction
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
delayed!

46. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Complement activation (active in both)
Fc

47. What is oprelevkin? and What is it used for?
Activates Th1 helper cells; Macrophages
MS - hay fever - SLE - goodpastures
Recom IL 11; thrombocytopenia
Liver! (they are proteins circulating in the blood)

48. The lymphocytes are ________ origin
Bind FcG for antibody dependent cellular cytotoxicity
mesenchymal
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

49. T/F B cells do not require a second signal
IgM and IgD
IgM and IgA
False! B cell class switching requires a second signal
MS

50. what happens in a deficiency of C1 esterase inhibitor? DAF?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Hereditary angioedema; PNH
Rheumatic arthritis