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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. in which immunodef order do you see a lot of pus? no pus?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Th cells fail to produce interferon gamma; a lot of IgE
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Alternative splicing of mRNA

2. What do multimeric antibodies require for assembly?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
A j chain
Negative!
pentamer

3. What is the pathogenesis of a hypersensitivity reaction?
Lymphocytes
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
Increases expression of MHC I and MHC II and also activates NK cells
Th2; Th1

4. IgG...
Kill them because they have CD16 on them that recognize the FcG portion
opsonizes
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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

5. What are some catalase positive organisms?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
S. aureus - E. Coli - aspergillus
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

6. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
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

7. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Acts as second signal on B cells to induce class switching to IgE and IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Complement activation (active in both)

8. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Interferon gamma; Th1
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
C5a
...

9. What is recomb beta interferon used for?
MS
By transcytosis
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Interferon gamma and IL 2

10. What are the two signals required for T cells? what happens after?
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!
Edema and necrosis in that region
Daclizumab; prevent ACUTE rejection of renal transplant

11. What is the main function of TNF alpha? How does it do this?
IL 5
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MS
Activate macrophages

12. What is the most common example of passive immunity?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Superficial inguinal
IgAs in mothers breast milk!

13. What is muromonab - CD3 (OKT3)
When you select for which MHC it will have; take out the lymphs that self react
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
TGF beta and IL 10
Antibody mediated cytotoxicity; either complement dependent or complement independent

14. What is the pathology in hyperacute transplant rejection?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
...

15. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
CRP - C3b - IgM
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
DM type I and RA

16. Which is the main antibody in the delayed or secondary response to an antigen?
CD56
IgG
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
encapsulated

17. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
...

18. 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
T cell activation; no with CD 4 or CD 8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A j chain

19. Type Iv hypersensitivity is...
Severe pyogenic infections early in life
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
delayed!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

20. 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
delayed!
Immunosuppression after kidney transplantation
Axillary

21. What is epo used for?
Anemias (esp due to renal failure)
Th cells fail to produce interferon gamma; a lot of IgE
Cyclosporine - OKT3
A recomb cytokine of IL 2; RCC and metastatic melanoma

22. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Interferon gamma; Th1
IgE
Anti TSh receptor

23. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
False! B cell class switching requires a second signal
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

24. What are the autoantibodies for autoimmune hepatitis?
2 heavy chains and two light chains
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti smooth muscle
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

25. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Not thymus - BM
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
When you select for which MHC it will have; take out the lymphs that self react

26. Name two endogenous pyrogens
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IL 1 and IL 6
MHC class molecules bind to KIRS or CD94 to prevent killing
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

27. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
T cell precursor
Alternative splicing of mRNA
MHC I - CD16 - CD56
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

28. What is passive immunity?
Its main effect is a defect in Ab opsonization for killing
Receiving preformed Antibodies
2 heavy chains and two light chains
S. aureus - E. Coli - aspergillus

29. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Antidote for digoxin intoxication
Remove encapsulated bacateria
Axillary
Th cells fail to produce interferon gamma; a lot of IgE

30. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti mitochondrial
Active; passive - fast but short half life (3 weeks!)
Chronic granulomatous disease

31. What are the autoantibodies for myasthenia gravis?
Th2; Th1
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti Ach receptor

32. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Wiskott Aldrich syndrome
except hyperacute
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Bind FcG for antibody dependent cellular cytotoxicity

33. So antibodies are the effectors for the humoral response. List some of their functions.
...
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)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

34. Name the three opsonins
Inferior mesenteric
CRP - C3b - IgM
Hereditary angioedema; PNH
Anti glutamate carboxylase and anti insulin

35. what will NK cells do to cells covered in IgG Ab? why?
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
Fab portion
Kill them because they have CD16 on them that recognize the FcG portion
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

36. What are the two signals required for Th1 cells? what happens after then activated?
pentamer
delayed!
Th2; Th1
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

37. What is the presentation of Brutons agammaglobulinemia?
Celiac
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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

38. What are MHC's necessary for? By themselves?
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
T cell activation; no with CD 4 or CD 8
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

39. which antibodies prevent antigens from binding mucosal surfaces?
IL 1 and IL 6
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
Anti topoisomerase
IgA

40. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
CD56
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Anti IF

41. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Popliteal
Activates Th1 helper cells; Macrophages
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
Liver! (they are proteins circulating in the blood)

42. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antibody mediated cytotoxicity; either complement dependent or complement independent
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

43. What is the toxicity of muromonab?
Tetanus - Botulinum - HBV - Rabies
Internal iliac
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Steroid responsive nephrotic syndrome

44. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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

45. What are the autoantibodies for systemic sclerosis?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti topoisomerase
T cell dysfunction
CD56

46. What lymph node drains the upper limb?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Axillary
isotype
Graves

47. What are the autoantibodies for type I diabetes mellitus?
B - T - and NK cells
IgG
Anti glutamate carboxylase and anti insulin
isotype

48. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cytokine IL 10 secreted by Th2
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

49. In general What are T cells good for?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti viral and anti tumor
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

50. give an example of how influenza does a major antigenic shift.
Local infection/inflammation; infection of the ln itself; metastasis
Influenza; antigenic shift; antigenic drift
RNA segment reassortment
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class