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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 cytokines are released by Th1 cells?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Interferon gamma and IL 2
pentamer

2. What does Interferon alpha and beta do? how?
Negative!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
MHC I; from RER with help of the B2 microglobulin
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

3. The secondary follicles have __________; primary follicles are dense
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
pale central germinal centers
Celiac
MHC class molecules bind to KIRS or CD94 to prevent killing

4. Give an example of someone who could get hyperacute transplant rejection.
Steroid responsive nephrotic syndrome
Previous transfusion; pregnant woman whose fetus had paternal antigens
All MHC 1/CD8
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 :(

5. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
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!
Previous transfusion; pregnant woman whose fetus had paternal antigens
Immunoflourescent staining of tissue biopsies

6. In general What are T cells good for?
Influenza; antigenic shift; antigenic drift
IgM and IgA
Anti viral and anti tumor
Sinusitis - otitis media - pneumonia

7. What are the two signals required for T cells? what happens after?
neutrophilia!
Negative!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
not Ab mediated

8. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti glutamate carboxylase and anti insulin
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 does granzyme do? who secretes it?
MS
Th2; Th1
Its a serine protease that activates apoptosis; NK and CD8
Fc

10. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
...
Active; passive - fast but short half life (3 weeks!)

11. The MALT/GALT are not...
encapsulated
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Anti viral and anti tumor
active complement pathway

12. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Anti mitochondrial
Negative selection
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

13. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
pathogenesis
Activates cytotoxic CD 8 T cells as second signal
Remove encapsulated bacateria
Glycoproteins; HLA

14. What does IL 10 do? who is secreted by?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
By transcytosis
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgM

15. What lymph node drains the thigh?
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
IgE; by activating eosinophils
IL 4 - 5 - 10 - 6
Superficial inguinal

16. What is the mechanism for sirolimus? what else it known as?
B - T - and NK cells
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
Humoral
Alternative splicing of mRNA

17. How is the antigen loaded onto a MHC II?
Anti topoisomerase
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

18. which of the hypersensitivity reactions is not Ab mediated?
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
Internal iliac
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Type IV

19. What is the pathogenesis of a hypersensitivity reaction?
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
Interferon gamma; Th1
CD56
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

20. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Type IV
IgA
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
pathogenesis

21. What is the pathogenesis of acute transplant rejection? When does it occur?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Activates Th1 helper cells; Macrophages

22. Give three examples of bacteria that use antigenic variation and how.
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
When you select for which MHC it will have; take out the lymphs that self react
IgE; by activating eosinophils
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

23. What are the autoantibodies for drug induced lupus?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antihistone
A chemotactic factor for neutrophils
Anti SS- A (anti RO) and Anti SS- B

24. The pathogenesis of contact dermatitis is ________ hypersensitivity
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
type four
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

25. What is the pathology in hyperacute transplant rejection?
IgM and IgG
Internal iliac
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
...

26. What are the autoantibodies for other vasculitides?
cannot cross placenta
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Celiac

27. which B and T cell disorder presents with specifically low IgM?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Alternative splicing of mRNA
acute phase reactants
Wiskott Aldrich syndrome

28. Which diseases are associated with DR5?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Pernicious Anemia and Hashimotos

29. What is the pathology of acute transplant rejection? is it reversible?
Complement activation (active in both)
Humoral
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
cannot cross placenta

30. What is the clinical use of Muromonab?
Chronic granulomatous disease
Immunosuppression after kidney transplantation
delayed!
IgAs in mothers breast milk!

31. The two heavy chains of an antibody contribute to the...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Fab portion
T

32. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Anti smooth muscle
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

33. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
cannot cross placenta
Macrophages - Dendritic cells - B cells
Interferon gamma and IL 2
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

34. which interleukin receptor is required for NK development? activation?
Alternative splicing of mRNA
Steroid responsive nephrotic syndrome
MHC I; from RER with help of the B2 microglobulin
IL 15; IL 12 - interferon Beta and interferon alpha

35. What is the toxicity of muromonab?
Popliteal
Th2; Th1
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

36. IgE has the ___________ in the serum
Superior mesenteric
Steroid responsive nephrotic syndrome
Negative selection
lowest concentration

37. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Stimulate the liver to release acute phase reactants
Negative nitroblue tetrazolium reduction test

38. What is muromonab - CD3 (OKT3)
IL 1 and IL 6
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Yes

39. is IgM an opsonizer?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
RNA segment reassortment
Celiac
Negative!

40. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Anemias (esp due to renal failure)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Steroid responsive nephrotic syndrome

41. IgM can exist as a _______ also
pentamer
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Steroid responsive nephrotic syndrome
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

42. other than C3a - what other complement acts as an anaphyloxin?
Para aortic
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
C5a

43. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Kill them because they have CD16 on them that recognize the FcG portion
Type IV
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

44. where do NK cells develop?
Immunoflourescent staining of tissue biopsies
Celiac
Not thymus - BM
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

45. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
SP infections
Hereditary angioedema; PNH
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

46. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Increases expression of MHC I and MHC II and also activates NK cells

47. What are MHC's necessary for? By themselves?
All MHC 1/CD8
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
T cell activation; no with CD 4 or CD 8

48. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
TGF beta and IL 10
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Superior mesenteric

49. What is the most common example of passive immunity?
pathogenesis
IgAs in mothers breast milk!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IL 5

50. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
pathogenesis
pale central germinal centers