Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. which of the hypersensitivity reactions is not Ab mediated?
Type IV
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Axillary
pentamer

2. What are the autoantibodies for goodpastures syndrome?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti alpha subunit 3 of collagen on type IV bm
IL 5
...

3. Which type of selection of thymic development provides central tolerance?
Negative selection
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superficial inguinal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

4. For which toxins are preformed antibodies (passive) given?
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
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
Tetanus - Botulinum - HBV - Rabies
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

5. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MS
Delayed type hypersensitivity
secondary

6. What is the presentation of common variable immunodef? and What are the labs?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
Anti Ach receptor
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

7. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
carboxy terminal
Paracortex
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

8. describe the pathogenesis of delayed type IV hypersensitivity
Sinusitis - otitis media - pneumonia
delayed!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
secondary

9. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Yes

10. What is an example of a parasite showing antigenic variation?
Anti Jo -1
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

11. What does IL 10 do? who is secreted by?
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IL 1 and IL 6
dimer

12. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cross link
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

13. What is the toxicity of azathioprine?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC I; from RER with help of the B2 microglobulin
IgM and IgD
...

14. To what portion of the Antibody do the complements bind?
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
Fc
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. Which diseases are associated with DR2?
Previous transfusion; pregnant woman whose fetus had paternal antigens
MS - hay fever - SLE - goodpastures
Cells that stil have weird parts of their membrane that macrophages usually bite off
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

16. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Local infection/inflammation; infection of the ln itself; metastasis
Previous transfusion; pregnant woman whose fetus had paternal antigens
Increases expression of MHC I and MHC II and also activates NK cells

17. A lymph node is a ________ lymphoid organ.
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
2 heavy chains and two light chains
secondary
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

18. What is the main function of IL 8?
A chemotactic factor for neutrophils
neutrophilia!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
B - T - and NK cells

19. What are the autoantibodies for primary biliary cirrhosis?
Cyclosporine - OKT3
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 :(
Anti mitochondrial
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

20. What does granulysin do?
Anti smooth muscle
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)
Antidote for digoxin intoxication

21. What is immune complex disease? give an example.
Steroid responsive nephrotic syndrome
Local infection/inflammation; infection of the ln itself; metastasis
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
The igA found in breast milk

22. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Sinusitis - otitis media - pneumonia
Activate macrophages
IL 3; supports growth and differentiation of bone marrow stem cells

23. How do you test for chronic granulomatous disease?
Humoral
IgM and IgD
Yes
Negative nitroblue tetrazolium reduction test

24. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgG
IgG
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

25. what cell surface marker is used for NK cells as it is unique to them?
If there is class switching and plasma cell production (that is when memory cells are produced)
CD56
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Steroid responsive nephrotic syndrome

26. 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?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Viral neutralization of igM and IgG!
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

27. What can cause a lymph node enlargement?
Histamine; post capillary venules - vasodilation
Remove encapsulated bacateria
Local infection/inflammation; infection of the ln itself; metastasis
Barrel hoop basement membrane fenestrations

28. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Viral neutralization of igM and IgG!
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Liver! (they are proteins circulating in the blood)

29. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Hereditary angioedema; PNH
All MHC 1/CD8

30. Which disease is associated with HLA A3?
TLR ad nuclear receptors
Hemochromatosis
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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

31. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
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
Inferior mesenteric
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

32. The two heavy chains of an antibody contribute to the...
Fab portion
Anemias (esp due to renal failure)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
opsonizes

33. What are the symptoms of serum sickness?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

34. What is the pathology of acute transplant rejection? is it reversible?
TNF alpha and IL1
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

35. What lymph node drains the breast?
Axillary
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Superficial inguinal
encapsulated

36. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Anti glutamate carboxylase and anti insulin
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
T cell activation; no with CD 4 or CD 8

37. 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
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
pentamer
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

38. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
except hyperacute
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)
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

39. What is the mechanism for sirolimus? what else it known as?
Anemias (esp due to renal failure)
Anti IF
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

40. What are the two signals required for T cells? what happens after?
T
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Antihistone
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

41. What does it mean if there are igM in the serum at birth?
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cell precursor
IgM and IgG
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

42. What is the clinical use of Muromonab?
Antidesmoglein
Immunosuppression after kidney transplantation
NK cells
By transcytosis

43. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Activates cytotoxic CD 8 T cells as second signal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
heavy chains

44. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Increases expression of MHC I and MHC II and also activates NK cells
Anti TSh receptor

45. what cell surface proteins are on all APCs?
MHC II - B7
Anti TSh receptor
Para aortic
not Ab mediated

46. What is the presentation of scid? treatment?
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgM and IgA
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti topoisomerase

47. What is digoxin immune Fab used for?
Stimulate the liver to release acute phase reactants
Antidote for digoxin intoxication
active complement pathway
Yes

48. What links the adaptive and innate immunity?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
mesenchymal
Complement activation (active in both)
IgA

49. 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Anti TSh receptor

50. what bacteria are a splenectomy patient most susceptible to? why?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L