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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. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Activates Th1 helper cells; Macrophages
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

2. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
IgM and IgD
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

3. What does interferon gamma do to be antiviral?
Lymphocytes
Increases expression of MHC I and MHC II and also activates NK cells
IL 5
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

4. The idiotype; the Fc portion determines the...
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
cannot cross placenta
isotype
Interferon gamma and IL 2

5. Monomer in circulation - ___ when secreted
dimer
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Antihistone
Sinusitis - otitis media - pneumonia

6. What does IL 5 do?
Anti topoisomerase
Liver! (they are proteins circulating in the blood)
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

7. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
RNA segment reassortment
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
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

8. hat is the presentation of Jobs syndrome or Hyper IgE?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Internal iliac
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

9. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 3; supports growth and differentiation of bone marrow stem cells
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. Which MHC presents intracellular peptides? how so?
Inferior mesenteric
not Ab mediated
MHC I; from RER with help of the B2 microglobulin
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

11. What is anergy? why does this occur?
T cell activation; no with CD 4 or CD 8
Local infection/inflammation; infection of the ln itself; metastasis
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

12. What lymph node drains the breast?
Thrombocytopenia
DM type I
mesenchymal
Axillary

13. What is hereditary angioedema? What are the C3 levels?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Anti U1 RNP (ribonucleoprotein)

14. What are the autoantibodies for sjorgens syndrome?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
pale central germinal centers
Anti SS- A (anti RO) and Anti SS- B
NK cells

15. which antibodies can bind complement?
IgAs in mothers breast milk!
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgM and IgG
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

16. What happens in a secondary follicle?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Negative selection
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

17. Which disease is associated with HLA A3?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
...
Hemochromatosis

18. What is recomb gamma interferon used for?
Lymphocytes
Steroid responsive nephrotic syndrome
Chronic granulomatous disease
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

19. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

20. What are the autoantibodies for Mixed connective tissue disease?
encapsulated
Basophils! THey want IG E class switch!
...
Anti U1 RNP (ribonucleoprotein)

21. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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

22. What are the main symptoms of T cell immunodeficiencies?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

23. What are the symptoms of serum sickness?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Superficial inguinal

24. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Recom IL 11; thrombocytopenia
A chemotactic factor for neutrophils

25. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
T cell activation; no with CD 4 or CD 8
pale central germinal centers
Fab portion

26. 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
Yes
No because no peptide fragment!
IgG

27. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Thrombocytopenia
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

28. What are the autoantibodies for myasthenia gravis?
IL 15; IL 12 - interferon Beta and interferon alpha
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Stimulate the liver to release acute phase reactants
Anti Ach receptor

29. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
Alternative splicing of mRNA
Paracortex; viral infection
Increases expression of MHC I and MHC II and also activates NK cells

30. Which HLA's are included in MHC I? MHC II?

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31. What are the three types of lymphocytes?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
pentamer
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
B - T - and NK cells

32. What is the toxicity of muromonab?
Edema and necrosis in that region
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
T cell precursor
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

33. What is the pathogenesis of a candida skin test?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Activates Th1 helper cells; Macrophages
Delayed type hypersensitivity

34. What is muromonab - CD3 (OKT3)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgAs in mothers breast milk!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Antihistone

35. What are the two signals required for B cell class switching? Which is the second signal?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Para aortic
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

36. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IgM and IgG
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

37. what cell surface proteins are on all APCs?
Anti topoisomerase
MHC II - B7
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

38. What does Interferon alpha and beta do? how?
T cell dysfunction
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Antidote for digoxin intoxication
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

39. What lymph node drains the upper limb?
Activate macrophages
Axillary
Secretory component
dimer

40. What are the autoantibodies for pernicious anemia?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
Anti IF
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

41. T/F B cells do not require a second signal
Pernicious Anemia and Hashimotos
Edema and necrosis in that region
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
False! B cell class switching requires a second signal

42. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgM and IgG
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

43. other than C3a - what other complement acts as an anaphyloxin?
C5a
The patient could become cyanotic in the OR!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

44. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Hereditary angioedema; PNH
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
IgM and IgA
Superficial inguinal

45. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Negative selection
Its main effect is a defect in Ab opsonization for killing
Th2; Th1
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

46. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

47. Give an example of someone who could get hyperacute transplant rejection.
RNA segment reassortment
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
C5a
Previous transfusion; pregnant woman whose fetus had paternal antigens

48. where are complements produced?
T
Liver! (they are proteins circulating in the blood)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

49. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
IgM and IgA
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 4
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

50. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Thrombocytopenia
The patient could become cyanotic in the OR!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy