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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 does Interferon alpha and beta do? how?
Inferior mesenteric
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
pentamer
MHC I - CD16 - CD56

2. What does interferon gamma do? What two type of cells does it attack mostly?
...
Activates Th1 helper cells; Macrophages
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

3. What kinds of receptors activate innate immunity?
IgM and IgG
No because no peptide fragment!
TLR ad nuclear receptors
Popliteal

4. What is the mechanism for sirolimus? what else it known as?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Chronic granulomatous disease
IgE
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

5. What are the main symptoms of B cell immunodeficiencies?
SP infections
pathogenesis
acute phase reactants
Anti mitochondrial

6. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
False! B cell class switching requires a second signal
Remove encapsulated bacateria
TGF beta and IL 10

7. What are the autoantibodies for Mixed connective tissue disease?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti U1 RNP (ribonucleoprotein)
Receiving preformed Antibodies
Anti IF

8. The pathogenesis of contact dermatitis is ________ hypersensitivity
Cytokine IL 10 secreted by Th2
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
Interferon gamma and IL 2
type four

9. __________ are a part of the innate system.
IgM
Remove encapsulated bacateria
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
NK cells

10. What are the autoantibodies for hashimotos?
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
Antimicrosomal and antithyroglobulin
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Its a serine protease that activates apoptosis; NK and CD8

11. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
TGF beta and IL 10
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

12. what mediates the type II hypersensitivity? What are the two different methods?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
S. aureus - E. Coli - aspergillus

13. give an example of how influenza does a major antigenic shift.
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
Hemochromatosis
S. aureus - E. Coli - aspergillus
RNA segment reassortment

14. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Antibody mediated cytotoxicity; either complement dependent or complement independent
not Ab mediated
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

15. what prevents NK cells from killing normal cells if their default is to kill?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti IF
Chronic granulomatous disease

16. What is the general structure of an Ab?
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
Immunoflourescent staining of tissue biopsies
Edema and necrosis in that region
2 heavy chains and two light chains

17. Type IV hypersensitivity is i...
Yes
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
not Ab mediated
A j chain

18. what cytokine does basophils secrete?
cannot cross placenta
IL 4
IL 3; supports growth and differentiation of bone marrow stem cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

19. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Axillary
IL 5
Th2; Th1

20. What is muromonab - CD3 (OKT3)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

21. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti viral and anti tumor
NK cells
CD56

22. What is the marginal zone of the spleen? what happens there?
Its main effect is a defect in Ab opsonization for killing
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Tetanus - Botulinum - HBV - Rabies
heavy chains

23. Only the _______ contribute to the Fc region
Acts as second signal on B cells to induce class switching to IgE and IgG
heavy chains
Carbohydrate
Anti Jo -1

24. What does granulysin do?
Humoral
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
type four
All MHC 1/CD8

25. What is the main cytokine released by T cells? What does it do
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Barrel hoop basement membrane fenestrations
Celiac
IL 3; supports growth and differentiation of bone marrow stem cells

26. How is sirolimus different from tacrolimus?
Anti Jo -1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

27. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti Ach receptor

28. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Sinusitis - otitis media - pneumonia
NK cells

29. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
By transcytosis
Delayed type hypersensitivity

30. What is the pathogenesis of acute transplant rejection? When does it occur?
Type IV
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
secondary

31. What are the major functions of Antibodies?
In the germinal center of secondary follicles (In the paler center)
Active; passive - fast but short half life (3 weeks!)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

32. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
IL 4 - 5 - 10 - 6
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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 :(
IL 5

33. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Increases expression of MHC I and MHC II and also activates NK cells
Anti alpha subunit 3 of collagen on type IV bm
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

34. 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
T
IL 15; IL 12 - interferon Beta and interferon alpha
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

35. What is Aldesleukin? What is it used for
IL 5
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
A recomb cytokine of IL 2; RCC and metastatic melanoma
Paracortex; viral infection

36. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Liver! (they are proteins circulating in the blood)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

37. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgM and IgD
IgE; by activating eosinophils

38. What does IL 10 do? who is secreted by?
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

39. What lymph node drains the testes?
IgM
Para aortic
Antidote for digoxin intoxication
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

40. What are MHC's necessary for? By themselves?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
T cell activation; no with CD 4 or CD 8
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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

41. What is recomb beta interferon used for?
MS
Antimicrosomal and antithyroglobulin
Negative nitroblue tetrazolium reduction test
Anti Jo -1

42. What are the symptoms of serum sickness?
Negative nitroblue tetrazolium reduction test
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Its main effect is a defect in Ab opsonization for killing

43. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
TLR ad nuclear receptors
...
MS - hay fever - SLE - goodpastures
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

44. What are the autoantibodies for sjorgens syndrome?
RNA segment reassortment
If there is class switching and plasma cell production (that is when memory cells are produced)
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti SS- A (anti RO) and Anti SS- B

45. What is the pathology of acute transplant rejection? is it reversible?
dimer
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
MHC I; from RER with help of the B2 microglobulin
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

46. What does IgA pick up from epithelial cells before being secreted?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Secretory component
S. aureus - E. Coli - aspergillus
Anti IF

47. What is the common variable immunodeficiency ? How is it different from Brutons?
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
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
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

48. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Activates cytotoxic CD 8 T cells as second signal
Axillary
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
except hyperacute

49. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

50. Describe the capsular structure of a lymph node; What are the functions of the LN?
IL 3; supports growth and differentiation of bone marrow stem cells
IL 4
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
RNA segment reassortment