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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. How do you test for type III hypersensitivity?
Inferior mesenteric
Para aortic
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Immunoflourescent staining of tissue biopsies

2. 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?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Thrombocytopenia
Negative!

3. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
TGF beta and IL 10
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
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
Barrel hoop basement membrane fenestrations

4. What lymph node drains the scrotum?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Superficial inguinal
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!
Chronic granulomatous disease

5. describe the classic complement pathway.
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
IgG
Fc
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

6. Which type of selection of thymic development provides central tolerance?
Negative selection
Negative nitroblue tetrazolium reduction test
Acts as second signal on B cells to induce class switching to IgE and IgG
T cell precursor

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
Histamine; post capillary venules - vasodilation
...
Severe pyogenic infections early in life

8. In thymic development - What is the positive selection? negative selections?
Alternative splicing of mRNA
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
When you select for which MHC it will have; take out the lymphs that self react

9. is IgM an opsonizer?
Negative!
Popliteal
IgG
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
CRP - C3b - IgM
opsonizes
No because no peptide fragment!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

11. A lymph node is a ________ lymphoid organ.
secondary
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
pentamer
Superficial inguinal

12. which type of immunity is slow but long lasting? as opposed to...
A - B - C; all the D's
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgM and IgD
Active; passive - fast but short half life (3 weeks!)

13. Name the three opsonins
Negative!
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)
CRP - C3b - IgM
Delayed type hypersensitivity

14. How is the antigen loaded onto a MHC II?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
Anti Ach receptor
Anti topoisomerase

15. What are the mediators that mast cells release?
Interferon gamma and IL 2
IgM and IgA
Glycoproteins; HLA
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

16. which antibody is involved in the primary response or immediate response to an antigen?
IgM
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
pentamer
Glycoproteins; HLA

17. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti mitochondrial
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Not thymus - BM
Antidote for digoxin intoxication

18. when can graft versus host disease? What is the result?
Active; passive - fast but short half life (3 weeks!)
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea

19. Name two endogenous pyrogens
IL 1 and IL 6
cannot cross placenta
...
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

20. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
except hyperacute
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

21. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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 (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Antihistone

22. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
...
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

23. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Paracortex; viral infection
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

24. What is muromonab - CD3 (OKT3)
Basophils! THey want IG E class switch!
A chemotactic factor for neutrophils
DM type I
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

25. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
Complement activation (active in both)
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
T cell dysfunction

26. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
MHC I; from RER with help of the B2 microglobulin
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

27. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Internal iliac
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

28. What does CD16 on NK cells do?
All MHC 1/CD8
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgM and IgA
Bind FcG for antibody dependent cellular cytotoxicity

29. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti Ach receptor
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

30. what characterizes an arthus reaction?
IgA
Antibody mediated cytotoxicity; either complement dependent or complement independent
Edema and necrosis in that region
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

31. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
...
Acts as second signal on B cells to induce class switching to IgE and IgG

32. How does the alternative pathway lead to MAC activation?
B - T - and NK cells
Rheumatic arthritis
Inferior mesenteric
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

33. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
T cell dysfunction
IgG
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

34. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Increases expression of MHC I and MHC II and also activates NK cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
heavy chains
Cells that stil have weird parts of their membrane that macrophages usually bite off

35. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
TGF beta and IL 10

36. What are the autoantibodies for systemic sclerosis?
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti topoisomerase

37. What are some sinopulmonary infections?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Sinusitis - otitis media - pneumonia
The patient could become cyanotic in the OR!

38. What lymph node drains the sigmoid colon?
DM type I
opsonizes
A recomb cytokine of IL 2; RCC and metastatic melanoma
Inferior mesenteric

39. which cytokine inhibits TH2 cells? secreted by who?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Cross link
Interferon gamma; Th1
IgE

40. What is the treatment of acute transplant rejection?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Cyclosporine - OKT3
Its a serine protease that activates apoptosis; NK and CD8

41. what cell surface marker is used for NK cells as it is unique to them?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IgA
Antidote for digoxin intoxication
CD56

42. What lymph node drains the duodenum - jejunum?
IgAs in mothers breast milk!
Superior mesenteric
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
The patient could become cyanotic in the OR!

43. IgM can exist as a _______ also
Activate macrophages
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
pentamer

44. What is the main function of TNF alpha? How does it do this?
Axillary
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
The patient could become cyanotic in the OR!

45. What are the cell surface proteins for Macrophages? which two are for opsonins?
The patient could become cyanotic in the OR!
Immunosuppression after kidney transplantation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Histamine; post capillary venules - vasodilation

46. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

47. IgE has the ___________ in the serum
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
lowest concentration
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

48. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

49. What is the clinical use of Muromonab?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antibody mediated cytotoxicity; either complement dependent or complement independent
neutrophilia!
Immunosuppression after kidney transplantation

50. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
heavy chains
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
pathogenesis