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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. Which cytokines do Th2 release and For what?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Superior mesenteric
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

2. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
...
Fc

3. where do NK cells develop?
Not thymus - BM
False! B cell class switching requires a second signal
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti alpha subunit 3 of collagen on type IV bm

4. What is recomb alpha interferon used for?
Anti viral and anti tumor
Acts as second signal on B cells to induce class switching to IgE and IgG
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
cannot cross placenta

5. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti viral and anti tumor
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
IgM and IgD

6. What is serum sickness? give an example.
Thrombocytopenia
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
In the germinal center of secondary follicles (In the paler center)
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

7. what secretes IL 4?
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!
Basophils! THey want IG E class switch!
Negative!
delayed!

8. What is passive immunity?
Receiving preformed Antibodies
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Paracortex; viral infection
The igA found in breast milk

9. Which disease is associated withB B27?
Antihistone
Barrel hoop basement membrane fenestrations
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Edema and necrosis in that region

10. What is an example of a parasite showing antigenic variation?
cannot cross placenta
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti mitochondrial
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

11. can igG cross the placenta?
carboxy terminal
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Yes

12. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
DM type I and RA
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 :(

13. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
Rheumatic arthritis
No because no peptide fragment!
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

14. What is the main cytokine that activates eosinophils?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
...
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 5

15. What is immune complex disease? give an example.
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Humoral
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

16. what happens in a deficiency of C1 esterase inhibitor? DAF?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Hereditary angioedema; PNH
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
A chemotactic factor for neutrophils

17. From where do cytokines come from?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Lymphocytes
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

18. IgM can fix complement but...
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
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
cannot cross placenta

19. Describe complement dependent Type II hypersensitivity. Give an example.
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
Hereditary angioedema; PNH

20. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
No because no peptide fragment!
Glycoproteins; HLA
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

21. Name the three opsonins
Antidote for digoxin intoxication
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Stimulate the liver to release acute phase reactants
CRP - C3b - IgM

22. What cytokines are released by Th1 cells?
MHC I - CD16 - CD56
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Interferon gamma and IL 2
SP infections

23. IgM can exist as a _______ also
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
pale central germinal centers
pentamer
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

24. what characterizes an arthus reaction?
Edema and necrosis in that region
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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 alpha subunit 3 of collagen on type IV bm

25. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Negative selection
mesenchymal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

26. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
MHC I; from RER with help of the B2 microglobulin
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!
In the germinal center of secondary follicles (In the paler center)
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

27. What are MHC's necessary for? By themselves?
Yes
Anti alpha subunit 3 of collagen on type IV bm
Active; passive - fast but short half life (3 weeks!)
T cell activation; no with CD 4 or CD 8

28. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
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
Daclizumab; prevent ACUTE rejection of renal transplant
MHC class molecules bind to KIRS or CD94 to prevent killing

29. Name two endogenous pyrogens
In the germinal center of secondary follicles (In the paler center)
IL 1 and IL 6
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
Viral neutralization of igM and IgG!

30. which cytokine inhibits TH2 cells? secreted by who?
delayed!
SP infections
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Interferon gamma; Th1

31. What are the two signals required for B cell class switching? Which is the second signal?
Yes
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Interferon gamma; Th1
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule

32. is IgM an opsonizer?
Negative!
Edema and necrosis in that region
Th2; Th1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

33. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Fc
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)
Interferon gamma; Th1
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

34. What are the autoantibodies for Mixed connective tissue disease?
IL 4 - 5 - 10 - 6
Anti U1 RNP (ribonucleoprotein)
In the germinal center of secondary follicles (In the paler center)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

35. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Cyclosporine - OKT3
TNF alpha and IL1
The igA found in breast milk
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

36. What happens in a secondary follicle?
T cell precursor
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Remove encapsulated bacateria
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

37. The alternative pathway is the only constutively...
Humoral
active complement pathway
MHC I; from RER with help of the B2 microglobulin
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

38. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
The igA found in breast milk
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
pathogenesis

39. 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
By transcytosis
Humoral
Its main effect is a defect in Ab opsonization for killing

40. What bugs can actually infect the lymph node itself?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

41. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgM and IgG
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Not thymus - BM

42. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
cannot cross placenta
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
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

43. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Bind FcG for antibody dependent cellular cytotoxicity
Negative nitroblue tetrazolium reduction test

44. hat is the presentation of Jobs syndrome or Hyper IgE?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Rheumatic arthritis
False! B cell class switching requires a second signal

45. 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
Liver! (they are proteins circulating in the blood)
Hemochromatosis
Receiving preformed Antibodies

46. A lymph node is a ________ lymphoid organ.
Anti SS- A (anti RO) and Anti SS- B
IgE
secondary
MHC I - CD16 - CD56

47. What are four results of a splenectomy?
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti smooth muscle

48. describe the pathogenesis of delayed type IV hypersensitivity
IL 15; IL 12 - interferon Beta and interferon alpha
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Superficial inguinal
Yes

49. What are the main symptoms of B cell immunodeficiencies?
SP infections
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cross link
Fab portion

50. What is oprelevkin? and What is it used for?
Anti alpha subunit 3 of collagen on type IV bm
Recom IL 11; thrombocytopenia
pentamer
Superficial inguinal