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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.
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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. Which type of selection of thymic development provides central tolerance?
Anemias (esp due to renal failure)
Anti TSh receptor
Negative selection
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

2. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Local infection/inflammation; infection of the ln itself; metastasis
Antihistone
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

3. What are the autoantibodies for pemphigus bulgaris?
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
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
Antidesmoglein
cannot cross placenta

4. 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
...
Liver! (they are proteins circulating in the blood)

5. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Wiskott Aldrich syndrome
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

6. Describe the Mannose Lectin pathway
heavy chains
not Ab mediated
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

7. 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?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

8. which antibodies can bind complement?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgM and IgA
IgM and IgG
Previous transfusion; pregnant woman whose fetus had paternal antigens

9. What is a factor that is a predictor for a bad transplantation?
carboxy terminal
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Previous transfusion; pregnant woman whose fetus had paternal antigens
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

10. What is the pathogenesis of a candida skin test?
IL 3; supports growth and differentiation of bone marrow stem cells
Delayed type hypersensitivity
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
dimer

11. Which is the main antibody in the delayed or secondary response to an antigen?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IgG
Its a serine protease that activates apoptosis; NK and CD8
Graves

12. Which diseases are associated with DR4?
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
DM type I and RA
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
2 heavy chains and two light chains

13. What lymph node drains the upper limb?
Axillary
Immunosuppression after kidney transplantation
Negative nitroblue tetrazolium reduction test
not Ab mediated

14. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anti mitochondrial

15. The MALT/GALT are not...
Complement activation (active in both)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
encapsulated
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

16. How is i Th1 helper cell inhibited?
...
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
Cytokine IL 10 secreted by Th2
By transcytosis

17. IgM can fix complement but...
T
SP infections
Interferon gamma; Th1
cannot cross placenta

18. Which disease is associated with DR7?
Interferon gamma; Th1
Steroid responsive nephrotic syndrome
Remove encapsulated bacateria
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

19. Type Iv hypersensitivity is...
Anti alpha subunit 3 of collagen on type IV bm
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Cytokine IL 10 secreted by Th2
delayed!

20. What is the pathogenesis of acute transplant rejection? When does it occur?
pale central germinal centers
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti IF
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

21. describe the pathogenesis of delayed type IV hypersensitivity
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

22. What are the major functions of Antibodies?
Th2; Th1
False! B cell class switching requires a second signal
IL 4
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

23. So antibodies are the effectors for the humoral response. List some of their functions.
Anti mitochondrial
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
S. aureus - E. Coli - aspergillus
Axillary

24. What type of side chains are found on Fc region of an antibody?
type four
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Carbohydrate
Activates cytotoxic CD 8 T cells as second signal

25. What are the function of B cells?
Th cells fail to produce interferon gamma; a lot of IgE
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

26. What are the autoantibodies for hashimotos?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antimicrosomal and antithyroglobulin
Anti IF
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

27. describe the classic complement pathway.
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MS
encapsulated
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

28. How does the alternative pathway lead to MAC activation?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
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
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

29. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
SP infections
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

30. 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
IgG
Sinusitis - otitis media - pneumonia
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

31. The Fc region is found on the...
MHC class molecules bind to KIRS or CD94 to prevent killing
Previous transfusion; pregnant woman whose fetus had paternal antigens
carboxy terminal
Th cells fail to produce interferon gamma; a lot of IgE

32. What are the main Cell surface proteins on T cells?
Anti glutamate carboxylase and anti insulin
If there is class switching and plasma cell production (that is when memory cells are produced)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Cells that stil have weird parts of their membrane that macrophages usually bite off

33. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anti TSh receptor
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

34. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
pathogenesis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

35. What is the marginal zone of the spleen? what happens there?
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
Celiac
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

36. what will NK cells do to cells covered in IgG Ab? why?
Antimicrosomal and antithyroglobulin
Kill them because they have CD16 on them that recognize the FcG portion
Bind FcG for antibody dependent cellular cytotoxicity
CD21 on B cells (although there is T cell lymphocytosis in EBV)

37. ________ regulate the cell mediated response.
Humoral
Negative!
Severe pyogenic infections early in life
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

38. Name 5 ways Antibody diversity is generated?
Anti Jo -1
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
Active; passive - fast but short half life (3 weeks!)
IL 5

39. What is hereditary angioedema? What are the C3 levels?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
NK cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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

40. What are the autoantibodies for wegeners granulomatosis?
Th2; Th1
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
By transcytosis
Local infection/inflammation; infection of the ln itself; metastasis

41. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Cross link
Alternative splicing of mRNA
type four
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

42. What are the autoantibodies for graves?
Anti alpha subunit 3 of collagen on type IV bm
Complement activation (active in both)
Anti TSh receptor
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

43. What are the main symptoms of B cell immunodeficiencies?
MHC I; from RER with help of the B2 microglobulin
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
SP infections
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

44. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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

45. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Carbohydrate
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

46. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
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
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

47. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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
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 :(
opsonizes
type four

48. What is Aldesleukin? What is it used for
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
DM type I
Para aortic
A recomb cytokine of IL 2; RCC and metastatic melanoma

49. What is the treatment of acute transplant rejection?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
type four
Cyclosporine - OKT3

50. What are the two signals required for Th1 cells? what happens after then activated?
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Antidesmoglein