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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. What is the clinical use for sirolimus? what should you combine it with?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Anti Jo -1

2. What are the cell surface proteins on NK cells?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Superficial inguinal
MHC I - CD16 - CD56
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

3. What are superantigens? give two examples.
Superficial inguinal
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
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

4. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Tetanus - Botulinum - HBV - Rabies
Remove encapsulated bacateria
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

5. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti IF
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

6. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
A chemotactic factor for neutrophils
S. aureus - E. Coli - aspergillus
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 15; IL 12 - interferon Beta and interferon alpha

7. For which toxins are preformed antibodies (passive) given?
Receiving preformed Antibodies
Tetanus - Botulinum - HBV - Rabies
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
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

8. What is the clinical use for azathioprine?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Viral neutralization of igM and IgG!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
...

9. How is the thymus organized? what happens in each section?
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
Alternative splicing of mRNA
...
A - B - C; all the D's

10. What does granulysin do?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

11. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
NK cells
By transcytosis
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

12. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Severe pyogenic infections early in life
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti SS- A (anti RO) and Anti SS- B
Hereditary angioedema; PNH

13. What does CD16 on NK cells do?
Type IV
Bind FcG for antibody dependent cellular cytotoxicity
A chemotactic factor for neutrophils
Remove encapsulated bacateria

14. What is the pathogenesis of acute transplant rejection? When does it occur?
A chemotactic factor for neutrophils
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

15. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

16. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
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
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
DM type I
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

17. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
mesenchymal
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

18. What lymph node drains the lateral side of the dorsum of the foot?
IgG
Popliteal
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

19. What is the late phase reaction of anaphylaxis allergy? what mediates it?
IL 15; IL 12 - interferon Beta and interferon alpha
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)
Anti smooth muscle
Cytokine IL 10 secreted by Th2

20. What are MHC's necessary for? By themselves?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
T cell activation; no with CD 4 or CD 8
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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

21. Which disease is associated with HLA A3?
Not thymus - BM
Hemochromatosis
Stimulate the liver to release acute phase reactants
Fc

22. What are the two signals to kill for NK cells?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

23. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
No because no peptide fragment!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IL 15; IL 12 - interferon Beta and interferon alpha
T cell precursor

24. 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?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti glutamate carboxylase and anti insulin
False! B cell class switching requires a second signal

25. Leukocyte adhesion defect presents with...
neutrophilia!
False! B cell class switching requires a second signal
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

26. What bugs can actually infect the lymph node itself?
No because no peptide fragment!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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

27. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
MS - hay fever - SLE - goodpastures
IgE
Superior mesenteric
...

28. in which immunodef order do you see a lot of pus? no pus?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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

29. What do mature naive B lymphocytes express?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgM and IgD
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

30. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Recom IL 11; thrombocytopenia
Anti smooth muscle
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

31. which antibody activate mast cells - basophils - and eosinophils?
Anti alpha subunit 3 of collagen on type IV bm
IgE
Stimulate the liver to release acute phase reactants
Influenza; antigenic shift; antigenic drift

32. Which disease is associated with B8?
except hyperacute
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
Sinusitis - otitis media - pneumonia
Graves

33. What is immune complex disease? give an example.
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Humoral
Negative nitroblue tetrazolium reduction test

34. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IgE
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

35. What lymph node drains the sigmoid colon?
Inferior mesenteric
CD56
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

36. other than C3a - what other complement acts as an anaphyloxin?
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
MHC II - B7
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
C5a

37. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Hemochromatosis
IgG
Daclizumab; prevent ACUTE rejection of renal transplant
A - B - C; all the D's

38. Type Iv hypersensitivity is...
Pernicious Anemia and Hashimotos
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
delayed!
lowest concentration

39. How does the alternative pathway lead to MAC activation?
Thrombocytopenia
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
In the germinal center of secondary follicles (In the paler center)

40. What are the autoantibodies for hashimotos?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Antimicrosomal and antithyroglobulin
carboxy terminal

41. What is the general structure of an Ab?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
False! B cell class switching requires a second signal
Previous transfusion; pregnant woman whose fetus had paternal antigens
2 heavy chains and two light chains

42. What lymph node drains the rectum (above the pectinate line)?
Yes
Th cells fail to produce interferon gamma; a lot of IgE
Internal iliac
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

43. What are the three types of APCs?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 4 - 5 - 10 - 6
neutrophilia!
Macrophages - Dendritic cells - B cells

44. What are C1 - C2 - C3 - C4 important for?
type four
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Barrel hoop basement membrane fenestrations
Viral neutralization of igM and IgG!

45. What are the autoantibodies for graves?
Local infection/inflammation; infection of the ln itself; metastasis
Anti TSh receptor
Activates Th1 helper cells; Macrophages
IL 5

46. The lymphocytes are ________ origin
mesenchymal
MHC class molecules bind to KIRS or CD94 to prevent killing
type four
IL 15; IL 12 - interferon Beta and interferon alpha

47. What is the receptor for EBV? On what cells is that located?
Antihistone
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anti viral and anti tumor
CD21 on B cells (although there is T cell lymphocytosis in EBV)

48. what ensure that a memory response is generated?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Wiskott Aldrich syndrome
If there is class switching and plasma cell production (that is when memory cells are produced)

49. what cell surface marker is used for NK cells as it is unique to them?
CD56
Lymphocytes
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Secretory component

50. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Para aortic
DM type I and RA
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

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USMLE Step 1 Immunology

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