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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 are howell jolly bodies?
IgM and IgG
Histamine; post capillary venules - vasodilation
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
TLR ad nuclear receptors

2. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
neutrophilia!
Severe pyogenic infections early in life
Steroid responsive nephrotic syndrome

3. What is recomb alpha interferon used for?
neutrophilia!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
False! B cell class switching requires a second signal
A chemotactic factor for neutrophils

4. What does IL 4 do?
MHC I - CD16 - CD56
Kill them because they have CD16 on them that recognize the FcG portion
Basophils! THey want IG E class switch!
Acts as second signal on B cells to induce class switching to IgE and IgG

5. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
carboxy terminal
Severe pyogenic infections early in life

6. What is serum sickness? give an example.
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
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
TNF alpha and IL1

7. How does complement link innate and adaptive?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Axillary
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

8. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Histamine; post capillary venules - vasodilation
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Activates Th1 helper cells; Macrophages

9. What is three common causes of severe combined immunodef? What is the result of all three?
Cyclosporine - OKT3
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

10. what happens in a deficiency of C1 esterase inhibitor? DAF?
IgM
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Hereditary angioedema; PNH
IL 5

11. hat is the presentation of Jobs syndrome or Hyper IgE?
Kill them because they have CD16 on them that recognize the FcG portion
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

12. What are the autoantibodies for hashimotos?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Chronic granulomatous disease
Kill them because they have CD16 on them that recognize the FcG portion
Antimicrosomal and antithyroglobulin

13. What lymph node drains the testes?
Para aortic
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
CD56
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

14. 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
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
T
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

15. What are the autoantibodies for myasthenia gravis?
IL 4 - 5 - 10 - 6
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
Anti Ach receptor
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

16. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
encapsulated
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

17. How is the thymus organized? what happens in each section?
Negative selection
Histamine; post capillary venules - vasodilation
IgE
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

18. What are the two signals required for B cell class switching? Which is the second signal?
Fab portion
IgG
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

19. Which disease is associated with DR3?
All MHC 1/CD8
DM type I
IL 4 - 5 - 10 - 6
Thrombocytopenia

20. give an example of how influenza does a major antigenic shift.
Delayed type hypersensitivity
Alternative splicing of mRNA
RNA segment reassortment
acute phase reactants

21. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Interferon gamma and IL 2
Activates Th1 helper cells; Macrophages
CD21 on B cells (although there is T cell lymphocytosis in EBV)

22. What are the autoantibodies for sjorgens syndrome?
Bind FcG for antibody dependent cellular cytotoxicity
Anti SS- A (anti RO) and Anti SS- B
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

23. Name the three opsonins
Anti Jo -1
CRP - C3b - IgM
IL 5
...

24. describe the pathogenesis of delayed type IV hypersensitivity
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
C5a
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

25. What are the autoantibodies for goodpastures syndrome?
2 heavy chains and two light chains
Anemias (esp due to renal failure)
Anti alpha subunit 3 of collagen on type IV bm
Previous transfusion; pregnant woman whose fetus had paternal antigens

26. What are the symptoms of serum sickness?
Humoral
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Th cells fail to produce interferon gamma; a lot of IgE
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

27. Which antibodies can be multimeric?
Anti IF
IgM and IgA
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

28. what will NK cells do to cells covered in IgG Ab? why?
Humoral
Bind FcG for antibody dependent cellular cytotoxicity
Its main effect is a defect in Ab opsonization for killing
Kill them because they have CD16 on them that recognize the FcG portion

29. where do somatic hypermutation and class switching occur?
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)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 4
In the germinal center of secondary follicles (In the paler center)

30. What is the pathogenesis of a hypersensitivity reaction?
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
IgA
Steroid responsive nephrotic syndrome

31. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Hereditary angioedema; PNH
Thrombocytopenia
active complement pathway

32. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Not thymus - BM
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Wiskott Aldrich syndrome

33. What are the cell surface proteins for Macrophages? which two are for opsonins?
Axillary
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
except hyperacute
Antimicrosomal and antithyroglobulin

34. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
except hyperacute
IL 15; IL 12 - interferon Beta and interferon alpha
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

35. Which type of selection of thymic development provides central tolerance?
Negative selection
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
IgG

36. 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?
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
Paracortex
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
In the germinal center of secondary follicles (In the paler center)

37. where are complements produced?
Liver! (they are proteins circulating in the blood)
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
MS - hay fever - SLE - goodpastures
Anti U1 RNP (ribonucleoprotein)

38. What does IL 10 do? who is secreted by?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Its main effect is a defect in Ab opsonization for killing
Thrombocytopenia
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

39. The Fc region is found on the...
Anti alpha subunit 3 of collagen on type IV bm
TLR ad nuclear receptors
Fab portion
carboxy terminal

40. What kinds of receptors activate innate immunity?
Barrel hoop basement membrane fenestrations
TLR ad nuclear receptors
If there is class switching and plasma cell production (that is when memory cells are produced)
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

41. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Superficial inguinal
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
IgG
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

42. What is the pathogenesis of acute transplant rejection? When does it occur?
Basophils! THey want IG E class switch!
False! B cell class switching requires a second signal
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Paracortex; viral infection

43. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MS
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

44. What is the most common selective Ig deficiency? What is the presentation?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti smooth muscle
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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

45. can igG cross the placenta?
pale central germinal centers
Yes
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)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

46. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
MHC II - B7
Daclizumab; prevent ACUTE rejection of renal transplant
Th2; Th1
No because no peptide fragment!

47. What type of fenestrations are found in the red pulp of the spleen?
Receiving preformed Antibodies
Barrel hoop basement membrane fenestrations
Anti SS- A (anti RO) and Anti SS- B
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

48. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
secondary
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Increases expression of MHC I and MHC II and also activates NK cells
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

49. what ensure that a memory response is generated?
S. aureus - E. Coli - aspergillus
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
NK cells
If there is class switching and plasma cell production (that is when memory cells are produced)

50. What are the autoantibodies for autoimmune hepatitis?
RNA segment reassortment
Anti smooth muscle
Anti viral and anti tumor
Anti mitochondrial