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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 does granulysin do?
neutrophilia!
Graves
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

2. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Pernicious Anemia and Hashimotos
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
IgA
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

3. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Superficial inguinal
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
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!
Glycoproteins; HLA

4. What is the pathogenesis of a hypersensitivity reaction?
Tetanus - Botulinum - HBV - Rabies
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
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

5. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
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
All MHC 1/CD8
IgM

6. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CRP - C3b - IgM
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
False! B cell class switching requires a second signal

7. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Negative selection

8. in which immunodef order do you see a lot of pus? no pus?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Daclizumab; prevent ACUTE rejection of renal transplant
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Rheumatic arthritis

9. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti Ach receptor
Paracortex

10. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
Active; passive - fast but short half life (3 weeks!)
opsonizes
Severe pyogenic infections early in life

11. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

12. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Active; passive - fast but short half life (3 weeks!)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Activates Th1 helper cells; Macrophages
MS - hay fever - SLE - goodpastures

13. 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)
Inferior mesenteric
IL 5
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

14. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
IL 15; IL 12 - interferon Beta and interferon alpha
Influenza; antigenic shift; antigenic drift
active complement pathway
Rheumatic arthritis

15. What are the autoantibodies for hashimotos?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anti IF
Antimicrosomal and antithyroglobulin
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

16. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Antidote for digoxin intoxication
MHC I; from RER with help of the B2 microglobulin

17. What do multimeric antibodies require for assembly?
Hereditary angioedema; PNH
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
A j chain

18. What are the main symptoms of B cell immunodeficiencies?
Anti IF
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
IgE; by activating eosinophils
SP infections

19. What is oprelevkin? and What is it used for?
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
Recom IL 11; thrombocytopenia
RNA segment reassortment
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

20. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Anti smooth muscle
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
Anti viral and anti tumor

21. Which antibodies can be multimeric?
IgM and IgA
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Barrel hoop basement membrane fenestrations
A chemotactic factor for neutrophils

22. where are complements produced?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
pentamer
Liver! (they are proteins circulating in the blood)
Acts as second signal on B cells to induce class switching to IgE and IgG

23. What is digoxin immune Fab used for?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Sinusitis - otitis media - pneumonia
Antidote for digoxin intoxication
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

24. What is epo used for?
Edema and necrosis in that region
Anemias (esp due to renal failure)
Glycoproteins; HLA
Anti TSh receptor

25. what cell surface marker is used for NK cells as it is unique to them?
Anti Ach receptor
Para aortic
CD56
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

26. What are target cells?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Wiskott Aldrich syndrome
Macrophages - Dendritic cells - B cells

27. What is the late phase reaction of anaphylaxis allergy? what mediates it?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Internal iliac
All MHC 1/CD8
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)

28. What is the toxicity of muromonab?
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Activate macrophages
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

29. What is a type I hypersensitivity reaction? What is atopic?
Antidesmoglein
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
cannot cross placenta

30. Which is the most abundant antibody in blood?
Liver! (they are proteins circulating in the blood)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgG
T cell activation; no with CD 4 or CD 8

31. Other than stimulating fever - what else does IL 6 do?
Immunosuppression after kidney transplantation
Stimulate the liver to release acute phase reactants
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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 :(

32. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Celiac
Edema and necrosis in that region
Glycoproteins; HLA
S. aureus - E. Coli - aspergillus

33. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti glutamate carboxylase and anti insulin
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

34. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Viral neutralization of igM and IgG!
Carbohydrate

35. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Hemochromatosis
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
A chemotactic factor for neutrophils

36. What are the function of B cells?
RNA segment reassortment
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 :(
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
T cell precursor

37. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Negative selection
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

38. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
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
TNF alpha and IL1
heavy chains

39. What is the treatment of acute transplant rejection?
cannot cross placenta
Cyclosporine - OKT3
Cytokine IL 10 secreted by Th2
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

40. What is the main function of interferons?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Daclizumab; prevent ACUTE rejection of renal transplant

41. What links the adaptive and innate immunity?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
CRP - C3b - IgM
Complement activation (active in both)
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

42. What is the pathogenesis of a candida skin test?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Delayed type hypersensitivity
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
...

43. describe the classic complement pathway.
Not thymus - BM
Inferior mesenteric
IgM and IgA
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

44. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
All MHC 1/CD8
IgAs in mothers breast milk!

45. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Daclizumab; prevent ACUTE rejection of renal transplant
Activate macrophages

46. What lymph node drains the stomach?
Celiac
IL 15; IL 12 - interferon Beta and interferon alpha
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
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin

47. So antibodies are the effectors for the humoral response. List some of their functions.
delayed!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti mitochondrial

48. Leukocyte adhesion defect presents with...
neutrophilia!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Kill them because they have CD16 on them that recognize the FcG portion

49. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Th cells fail to produce interferon gamma; a lot of IgE

50. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti Ach receptor
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MHC I; from RER with help of the B2 microglobulin