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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 the autoantibodies for myasthenia gravis?
DM type I
Anti Ach receptor
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

2. which antibodies can bind complement?
A recomb cytokine of IL 2; RCC and metastatic melanoma
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgM and IgG

3. 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).
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!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Anti U1 RNP (ribonucleoprotein)

4. which of the transplant rejections is antibody mediated? why does it occur?
Daclizumab; prevent ACUTE rejection of renal transplant
TLR ad nuclear receptors
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

5. Which are the only two antiinflammatory cytokines?
Remove encapsulated bacateria
TGF beta and IL 10
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
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

6. What is the pathology of acute transplant rejection? is it reversible?
acute phase reactants
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

7. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
acute phase reactants
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

8. What portion of the lymph node is not well developed in DiGeorge Syndrome?
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
Paracortex
Anti alpha subunit 3 of collagen on type IV bm
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

9. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Fab portion
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. A lymph node is a ________ lymphoid organ.
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
secondary
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
Barrel hoop basement membrane fenestrations

11. What is the toxicity of muromonab?
encapsulated
Anti glutamate carboxylase and anti insulin
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anti SS- A (anti RO) and Anti SS- B

12. can igG cross the placenta?
acute phase reactants
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Yes

13. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
T cell activation; no with CD 4 or CD 8
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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

14. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
pathogenesis
cannot cross placenta

15. where are complements produced?
Hereditary angioedema; PNH
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Liver! (they are proteins circulating in the blood)
encapsulated

16. what happens in a deficiency of C1 esterase inhibitor? DAF?
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
IgA
Hereditary angioedema; PNH
MHC II - B7

17. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
A - B - C; all the D's
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

18. Which cytokines do Th2 release and For what?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Axillary

19. 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)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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

20. In general What are T cells good for?
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 :(
RNA segment reassortment
Anti viral and anti tumor
Superior mesenteric

21. 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?
RNA segment reassortment
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 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
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

22. What happens in a secondary follicle?
Yes
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Paracortex
IgA

23. Describe complement dependent Type II hypersensitivity. Give an example.
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Antidesmoglein

24. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
not Ab mediated
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Tetanus - Botulinum - HBV - Rabies
Anti mitochondrial

25. What do mature naive B lymphocytes express?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
IgM and IgD
Anti Jo -1

26. 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?
MS
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Negative selection

27. which cells have more complete tolerance - B or T cells?
Anti Ach receptor
T
The patient could become cyanotic in the OR!
MHC I - CD16 - CD56

28. Which diseases are associated with DR5?
IgA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Pernicious Anemia and Hashimotos
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

29. What are some sinopulmonary infections?
lowest concentration
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Sinusitis - otitis media - pneumonia
C5a

30. when can graft versus host disease? What is the result?
Delayed type hypersensitivity
except hyperacute
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

31. What is the clinical use for azathioprine?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Histamine; post capillary venules - vasodilation
IgAs in mothers breast milk!
...

32. Name the three opsonins
CRP - C3b - IgM
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anemias (esp due to renal failure)

33. What are the labs in brutons agammaglobulinemia?
dimer
Wiskott Aldrich syndrome
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

34. What is the presentation of Brutons agammaglobulinemia?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

35. What is the presentation of hyperIgM syndrome?
secondary
IL 15; IL 12 - interferon Beta and interferon alpha
Acts as second signal on B cells to induce class switching to IgE and IgG
Severe pyogenic infections early in life

36. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
A chemotactic factor for neutrophils
IgM and IgA
Negative nitroblue tetrazolium reduction test
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

37. which cytokine inhibits TH2 cells? secreted by who?
Anemias (esp due to renal failure)
Popliteal
Interferon gamma; Th1
TNF alpha and IL1

38. Give three examples of bacteria that use antigenic variation and how.
CRP - C3b - IgM
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
Fc
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

39. The lymphocytes are ________ origin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
mesenchymal

40. For which toxins are preformed antibodies (passive) given?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
T cell activation; no with CD 4 or CD 8
Tetanus - Botulinum - HBV - Rabies

41. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Cyclosporine - OKT3
Paracortex; viral infection
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Previous transfusion; pregnant woman whose fetus had paternal antigens

42. How fast does it occur?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
The patient could become cyanotic in the OR!

43. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

44. What is the pathology seen in chronic transplant rejection?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Activates cytotoxic CD 8 T cells as second signal
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

45. What is Aldesleukin? What is it used for
Paracortex
A recomb cytokine of IL 2; RCC and metastatic melanoma
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Para aortic

46. What are the autoantibodies for pernicious anemia?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti IF
Paracortex
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

47. What are the autoantibodies for Celiac disease?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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

48. What are the function of B cells?
C5a
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
CRP - C3b - IgM
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

49. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgA

50. Describe the capsular structure of a lymph node; What are the functions of the LN?
Viral neutralization of igM and IgG!
neutrophilia!
Cytokine IL 10 secreted by Th2
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