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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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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 is the pathogenesis of HyperIgE syndrome? What are the labs?
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)
Activates cytotoxic CD 8 T cells as second signal
Viral neutralization of igM and IgG!
Th cells fail to produce interferon gamma; a lot of IgE

2. What are the function of B cells?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Not thymus - BM
Activate macrophages
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

3. what characterizes an arthus reaction?
Edema and necrosis in that region
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Basophils! THey want IG E class switch!

4. 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?
MHC II - B7
All MHC 1/CD8
Chronic granulomatous disease
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

5. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Rheumatic arthritis

6. what bacteria are a splenectomy patient most susceptible to? why?
Daclizumab; prevent ACUTE rejection of renal transplant
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen

7. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Anti alpha subunit 3 of collagen on type IV bm
IL 5
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

8. Which MHC presents intracellular peptides? how so?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
MHC I; from RER with help of the B2 microglobulin
Type IV
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

9. The lymphocytes are ________ origin
Antihistone
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
mesenchymal

10. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Type IV
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
Pernicious Anemia and Hashimotos

11. What does CD16 on NK cells do?
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
Severe pyogenic infections early in life
Bind FcG for antibody dependent cellular cytotoxicity
delayed!

12. Which is the main antibody that provides passive immunity to infants?
Superior mesenteric
Th cells fail to produce interferon gamma; a lot of IgE
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IgG

13. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
delayed!
heavy chains
except hyperacute
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

14. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
acute phase reactants
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
secondary

15. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Celiac
Antibody mediated cytotoxicity; either complement dependent or complement independent
By transcytosis

16. 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)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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 :(
Sinusitis - otitis media - pneumonia

17. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Tetanus - Botulinum - HBV - Rabies
Acts as second signal on B cells to induce class switching to IgE and IgG
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

18. What are the labs in brutons agammaglobulinemia?
Activate macrophages
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
except hyperacute
delayed!

19. What are the autoantibodies for graves?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti TSh receptor
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

20. What is the pathology seen in chronic transplant rejection?
Histamine; post capillary venules - vasodilation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Type IV
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

21. What is the main cytokine released by T cells? What does it do
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Viral neutralization of igM and IgG!
IL 3; supports growth and differentiation of bone marrow stem cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

22. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Internal iliac
acute phase reactants
Rheumatic arthritis

23. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
MHC I; from RER with help of the B2 microglobulin

24. What links the adaptive and innate immunity?
Celiac
Anti SS- A (anti RO) and Anti SS- B
Th2; Th1
Complement activation (active in both)

25. Describe the capsular structure of a lymph node; What are the functions of the LN?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Antihistone

26. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Interferon gamma and IL 2
IL 1 and IL 6

27. What are the autoantibodies for other vasculitides?
Remove encapsulated bacateria
Superficial inguinal
Internal iliac
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

28. Which helper T cells' development is induced by IL 4? IL 12?
IgE
Th2; Th1
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
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

29. What are the autoantibodies for primary biliary cirrhosis?
MHC I; from RER with help of the B2 microglobulin
Anti mitochondrial
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
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

30. What is epo used for?
IL 4 - 5 - 10 - 6
Anemias (esp due to renal failure)
neutrophilia!
Barrel hoop basement membrane fenestrations

31. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Antihistone
...
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
not Ab mediated

32. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Para aortic
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti SS- A (anti RO) and Anti SS- B

33. What are the autoantibodies for hashimotos?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Sinusitis - otitis media - pneumonia
Antimicrosomal and antithyroglobulin

34. Which disease is associated with HLA A3?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Hemochromatosis
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

35. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
pale central germinal centers
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
Severe pyogenic infections early in life

36. what prevents NK cells from killing normal cells if their default is to kill?
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
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti alpha subunit 3 of collagen on type IV bm
IL 4

37. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgG

38. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
heavy chains

39. which cytokine inhibits TH2 cells? secreted by who?
IgA
Interferon gamma; Th1
Remove encapsulated bacateria
Steroid responsive nephrotic syndrome

40. What does IL 10 do? who is secreted by?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Remove encapsulated bacateria
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

41. What is oprelevkin? and What is it used for?
Remove encapsulated bacateria
Recom IL 11; thrombocytopenia
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

42. What are the autoantibodies for pemphigus bulgaris?
not Ab mediated
Anti glutamate carboxylase and anti insulin
Antidesmoglein
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 :(

43. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Histamine; post capillary venules - vasodilation
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
CD56

44. Name two endogenous pyrogens
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IL 5
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 1 and IL 6

45. How does the alternative pathway lead to MAC activation?
Immunosuppression after kidney transplantation
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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

46. What is chronic mucocutaneous candidiasis d/t?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
T cell dysfunction
IgM and IgG
IgM and IgD

47. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Superior mesenteric
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
All MHC 1/CD8

48. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
T cell activation; no with CD 4 or CD 8
Previous transfusion; pregnant woman whose fetus had paternal antigens
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

49. What are howell jolly bodies?
Rheumatic arthritis
Anti glutamate carboxylase and anti insulin
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

50. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
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 :(
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
Histamine; post capillary venules - vasodilation
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)