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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.
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1. What is the main function of IL 12? other than macrophages who else can release IL 12?
IgAs in mothers breast milk!
RNA segment reassortment
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

2. What is the most common example of passive immunity?
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
RNA segment reassortment
IgAs in mothers breast milk!
Anti Ach receptor

3. Which disease is associated with DR3?
DM type I
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
...
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

4. What is recomb gamma interferon used for?
Chronic granulomatous disease
...
Cells that stil have weird parts of their membrane that macrophages usually bite off
Tetanus - Botulinum - HBV - Rabies

5. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Activate macrophages
Axillary
Stimulate the liver to release acute phase reactants

6. what secretes IL 4?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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)
Basophils! THey want IG E class switch!
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

7. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Edema and necrosis in that region
pale central germinal centers
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

8. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Glycoproteins; HLA
Anti U1 RNP (ribonucleoprotein)

9. Give three examples of bacteria that use antigenic variation and how.
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

10. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Bind FcG for antibody dependent cellular cytotoxicity
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Th cells fail to produce interferon gamma; a lot of IgE
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

11. What are the autoantibodies for myasthenia gravis?
Barrel hoop basement membrane fenestrations
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
not Ab mediated
Anti Ach receptor

12. What type of fenestrations are found in the red pulp of the spleen?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Barrel hoop basement membrane fenestrations
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

13. in which immunodef order do you see a lot of pus? no pus?
mesenchymal
Wiskott Aldrich syndrome
Antimicrosomal and antithyroglobulin
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

14. other than mediating shock - what else does TNF alpha do? who releases it mainly?
IgG
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Activates Th1 helper cells; Macrophages

15. Type Iv hypersensitivity is...
delayed!
IgE
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

16. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Superficial inguinal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
DM type I and RA

17. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Antihistone
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

18. is IgM an opsonizer?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Negative!
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

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

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20. what characterizes an arthus reaction?
Edema and necrosis in that region
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IL 5
A - B - C; all the D's

21. What is the mechanism for sirolimus? what else it known as?
IgM
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
pathogenesis
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

22. What is recomb alpha interferon used for?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Negative nitroblue tetrazolium reduction test
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
T cell dysfunction

23. What is the main cytokine released by T cells? What does it do
Para aortic
MHC I; from RER with help of the B2 microglobulin
Superior mesenteric
IL 3; supports growth and differentiation of bone marrow stem cells

24. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
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
Anti smooth muscle
lowest concentration

25. describe the pathogenesis of delayed type IV hypersensitivity
MHC class molecules bind to KIRS or CD94 to prevent killing
isotype
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

26. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Interferon gamma and IL 2
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

27. What are C1 - C2 - C3 - C4 important for?
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
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
Viral neutralization of igM and IgG!
SP infections

28. What is the autoantibody for SLE that is nonspecific? Specific?
Anti IF
Hemochromatosis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

29. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
isotype
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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

30. Which antibody mediates immunity to worms? how?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
IgE; by activating eosinophils
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

31. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

32. What are the main symptoms of T cell immunodeficiencies?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti alpha subunit 3 of collagen on type IV bm
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

33. What do multimeric antibodies require for assembly?
Bind FcG for antibody dependent cellular cytotoxicity
Superficial inguinal
A j chain
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

34. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Basophils! THey want IG E class switch!
Complement activation (active in both)
Popliteal

35. What are the autoantibodies for Mixed connective tissue disease?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti U1 RNP (ribonucleoprotein)
Anti mitochondrial

36. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Activate macrophages
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

37. What is the treatment of acute transplant rejection?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cyclosporine - OKT3
Internal iliac
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

38. Which disease is associated with HLA A3?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Hemochromatosis
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
Increases expression of MHC I and MHC II and also activates NK cells

39. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Cytokine IL 10 secreted by Th2
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Alternative splicing of mRNA
The igA found in breast milk

40. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Thrombocytopenia
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cross link

41. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
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)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

42. What does IL 2 do?
Steroid responsive nephrotic syndrome
Cytokine IL 10 secreted by Th2
Activates cytotoxic CD 8 T cells as second signal
IL 4 - 5 - 10 - 6

43. What does granzyme do? who secretes it?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Internal iliac
Its a serine protease that activates apoptosis; NK and CD8

44. What lymph node drains the rectum (above the pectinate line)?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Internal iliac
Increases expression of MHC I and MHC II and also activates NK cells

45. hat is the presentation of Jobs syndrome or Hyper IgE?
IL 1 and IL 6
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

46. Only the _______ contribute to the Fc region
T cell activation; no with CD 4 or CD 8
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Active; passive - fast but short half life (3 weeks!)
heavy chains

47. What happens in a secondary follicle?
Thrombocytopenia
No because no peptide fragment!
Superficial inguinal
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

48. What does Interferon alpha and beta do? how?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
RNA segment reassortment
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

49. What is hereditary angioedema? What are the C3 levels?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Bind FcG for antibody dependent cellular cytotoxicity
MHC I; from RER with help of the B2 microglobulin

50. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IgM and IgD
Rheumatic arthritis
Immunosuppression after kidney transplantation