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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 are the three types of APCs?
If there is class switching and plasma cell production (that is when memory cells are produced)
Macrophages - Dendritic cells - B cells
...
Carbohydrate

2. What is the toxicity of muromonab?
Remove encapsulated bacateria
Basophils! THey want IG E class switch!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IL 15; IL 12 - interferon Beta and interferon alpha

3. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
A chemotactic factor for neutrophils
2 heavy chains and two light chains

4. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Yes
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

5. What are the autoantibodies for type I diabetes mellitus?
If there is class switching and plasma cell production (that is when memory cells are produced)
Glycoproteins; HLA
Anti glutamate carboxylase and anti insulin
Fc

6. What is three common causes of severe combined immunodef? What is the result of all three?
Activates Th1 helper cells; Macrophages
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MHC II - B7

7. What are the major functions of Antibodies?
Pernicious Anemia and Hashimotos
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Antimicrosomal and antithyroglobulin
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

8. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti glutamate carboxylase and anti insulin

9. What are the autoantibodies for other vasculitides?
Superior mesenteric
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

10. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
Liver! (they are proteins circulating in the blood)

11. What is the presentation of common variable immunodef? and What are the labs?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
acute phase reactants

12. Name two endogenous pyrogens
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Alternative splicing of mRNA
Anti TSh receptor
IL 1 and IL 6

13. What lymph node drains the upper limb?
Axillary
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

14. What are the two signals required for T cells? what happens after?
Fc
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Paracortex; viral infection
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

15. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
MS
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 :(
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

16. What are the main symptoms of T cell immunodeficiencies?
Tetanus - Botulinum - HBV - Rabies
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction

17. What is the main cytokine that activates eosinophils?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 5
mesenchymal

18. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
dimer
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

19. The idiotype; the Fc portion determines the...
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
isotype
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Barrel hoop basement membrane fenestrations

20. In thymic development - What is the positive selection? negative selections?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Chronic granulomatous disease
When you select for which MHC it will have; take out the lymphs that self react
IL 4

21. How does complement link innate and adaptive?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
2 heavy chains and two light chains
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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 :(

22. What is recomb beta interferon used for?
Activates Th1 helper cells; Macrophages
MS
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Tetanus - Botulinum - HBV - Rabies

23. What does interferon gamma do? What two type of cells does it attack mostly?
The patient could become cyanotic in the OR!
IL 4 - 5 - 10 - 6
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

24. What are the main Cell surface proteins on T cells?
not Ab mediated
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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

25. What is the marginal zone of the spleen? what happens there?
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)
cannot cross placenta
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
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

26. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IL 3; supports growth and differentiation of bone marrow stem cells
Kill them because they have CD16 on them that recognize the FcG portion
Increases expression of MHC I and MHC II and also activates NK cells

27. Which helper T cells' development is induced by IL 4? IL 12?
Hemochromatosis
IL 3; supports growth and differentiation of bone marrow stem cells
pathogenesis
Th2; Th1

28. Which is the main antibody that provides passive immunity to infants?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Thrombocytopenia
IgG
heavy chains

29. which of the hypersensitivity reactions is not Ab mediated?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Type IV
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

30. What is passive immunity?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
Type IV
Receiving preformed Antibodies

31. other than eat and bite RBCs what else do Macrophages of spleen do>
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Receiving preformed Antibodies
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!
Remove encapsulated bacateria

32. What is the clinical use for azathioprine?
IgE; by activating eosinophils
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
...

33. Leukocyte adhesion defect presents with...
Alternative splicing of mRNA
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
neutrophilia!
Axillary

34. Monomer in circulation - ___ when secreted
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
cannot cross placenta
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
dimer

35. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
Anti IF
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

36. other than C3a - what other complement acts as an anaphyloxin?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
C5a
Local infection/inflammation; infection of the ln itself; metastasis

37. What are the autoantibodies for primary biliary cirrhosis?
IgE; by activating eosinophils
type four
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti mitochondrial

38. What does IgA pick up from epithelial cells before being secreted?
Antidesmoglein
acute phase reactants
Secretory component
active complement pathway

39. which interleukin receptor is required for NK development? activation?
Immunosuppression after kidney transplantation
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
IL 15; IL 12 - interferon Beta and interferon alpha
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

40. What are MHC's necessary for? By themselves?
No because no peptide fragment!
Superficial inguinal
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
T cell activation; no with CD 4 or CD 8

41. What are howell jolly bodies?
Chronic granulomatous disease
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Basophils! THey want IG E class switch!

42. what prevents NK cells from killing normal cells if their default is to kill?
A j chain
Cells that stil have weird parts of their membrane that macrophages usually bite off
MHC class molecules bind to KIRS or CD94 to prevent killing
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

43. The two heavy chains of an antibody contribute to the...
Tetanus - Botulinum - HBV - Rabies
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
T
Fab portion

44. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Antibody mediated cytotoxicity; either complement dependent or complement independent
The patient could become cyanotic in the OR!
Activates Th1 helper cells; Macrophages
MS - hay fever - SLE - goodpastures

45. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
DM type I and RA

46. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Recom IL 11; thrombocytopenia
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

47. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
Graves
IgM and IgG
MS - hay fever - SLE - goodpastures

48. What is the treatment of acute transplant rejection?
Superficial inguinal
Cyclosporine - OKT3
Chronic granulomatous disease
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

49. 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?
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
By transcytosis
IL 4
IL 5

50. What does interferon gamma do to be antiviral?
Antidote for digoxin intoxication
Increases expression of MHC I and MHC II and also activates NK cells
No because no peptide fragment!
A - B - C; all the D's