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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.
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. what will NK cells do to cells covered in IgG Ab? why?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Kill them because they have CD16 on them that recognize the FcG portion

2. Which disease is associated withB B27?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Kill them because they have CD16 on them that recognize the FcG portion
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

3. Which is the main antibody in the delayed or secondary response to an antigen?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Antimicrosomal and antithyroglobulin

4. What is the presentation of common variable immunodef? and What are the labs?
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
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
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
B - T - and NK cells

5. What is the pathology of acute transplant rejection? is it reversible?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
By transcytosis
Influenza; antigenic shift; antigenic drift
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

6. What are the main cell surface proteins on B cells?
neutrophilia!
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
pathogenesis
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

7. How is the antigen loaded onto a MHC II?
Kill them because they have CD16 on them that recognize the FcG portion
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 4
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

8. What lymph node drains the anal canal (below the pectinate line)?
If there is class switching and plasma cell production (that is when memory cells are produced)
encapsulated
Superficial inguinal
Antihistone

9. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Glycoproteins; HLA
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
not Ab mediated
dimer

10. What is filgrastim and sargramostim? and What is it used for?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Complement activation (active in both)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

11. What is the pathogenesis of a candida skin test?
TLR ad nuclear receptors
Secretory component
Delayed type hypersensitivity
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!

12. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Basophils! THey want IG E class switch!
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t

13. What are the autoantibodies for systemic sclerosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Delayed type hypersensitivity
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
Anti topoisomerase

14. Which disease is associated with HLA A3?
not Ab mediated
Antidote for digoxin intoxication
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
Hemochromatosis

15. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgAs in mothers breast milk!
encapsulated

16. 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?
Pernicious Anemia and Hashimotos
pathogenesis
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

17. What are the main symptoms of B cell immunodeficiencies?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cytokine IL 10 secreted by Th2
SP infections

18. What is the main cytokine released by T cells? What does it do
opsonizes
IL 3; supports growth and differentiation of bone marrow stem cells
Negative!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

19. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Thrombocytopenia
Anemias (esp due to renal failure)
pentamer
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

20. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
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
Anti viral and anti tumor
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

21. Only the _______ contribute to the Fc region
heavy chains
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!
Interferon gamma; Th1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

22. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
DM type I and RA
RNA segment reassortment

23. What does CD16 on NK cells do?
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
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
Bind FcG for antibody dependent cellular cytotoxicity
Anti smooth muscle

24. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Negative selection
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

25. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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)
Yes

26. What is a factor that is a predictor for a bad transplantation?
Celiac
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

27. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
DM type I
cannot cross placenta
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

28. What lymph node drains the sigmoid colon?
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Inferior mesenteric
acute phase reactants
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

29. What are the autoantibodies for drug induced lupus?
isotype
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Stimulate the liver to release acute phase reactants
Antihistone

30. IgG...
opsonizes
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Anti U1 RNP (ribonucleoprotein)
Anti Jo -1

31. What lymph node drains the scrotum?
Superficial inguinal
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

32. Which is the main antibody that provides passive immunity to infants?
IgG
IgA
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
Anemias (esp due to renal failure)

33. which antibody is involved in the primary response or immediate response to an antigen?
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
IgM
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

34. What is recomb gamma interferon used for?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Chronic granulomatous disease
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

35. The MALT/GALT are not...
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
encapsulated
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
TNF alpha and IL1

36. To what portion of the Antibody do the complements bind?
The patient could become cyanotic in the OR!
Fc
A - B - C; all the D's
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

37. What is the treatment of acute transplant rejection?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Its a serine protease that activates apoptosis; NK and CD8
Acts as second signal on B cells to induce class switching to IgE and IgG
Cyclosporine - OKT3

38. 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
MS
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
dimer

39. What are the autoantibodies for primary biliary cirrhosis?
Thrombocytopenia
Anti mitochondrial
Antihistone
pathogenesis

40. How does the alternative pathway lead to MAC activation?
IgA
TNF alpha and IL1
Hereditary angioedema; PNH
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

41. What are the autoantibodies for sjorgens syndrome?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti SS- A (anti RO) and Anti SS- B
Axillary
Anti viral and anti tumor

42. What are some catalase positive organisms?
...
type four
S. aureus - E. Coli - aspergillus
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

43. Which antibody mediates immunity to worms? how?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgE; by activating eosinophils
Daclizumab; prevent ACUTE rejection of renal transplant
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

44. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
Rheumatic arthritis
A j chain
Antihistone

45. What are the two signals to kill for NK cells?
CD56
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
CD21 on B cells (although there is T cell lymphocytosis in EBV)

46. What is the most common example of passive immunity?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgAs in mothers breast milk!

47. The alternative pathway is the only constutively...
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
active complement pathway
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
TGF beta and IL 10

48. can igG cross the placenta?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Yes
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Acts as second signal on B cells to induce class switching to IgE and IgG

49. What lymph node drains the thigh?
CRP - C3b - IgM
Superficial inguinal
Steroid responsive nephrotic syndrome
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

50. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Daclizumab; prevent ACUTE rejection of renal transplant
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!
MHC II - B7
Lymphocytes