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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. what cell surface proteins are on all APCs?
Stimulate the liver to release acute phase reactants
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC II - B7
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

2. Describe the Mannose Lectin pathway
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
Alternative splicing of mRNA
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

3. which of the transplant rejections is antibody mediated? why does it occur?
Cyclosporine - OKT3
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

4. What are the autoantibodies for goodpastures syndrome?
Anti SS- A (anti RO) and Anti SS- B
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Cross link
Anti alpha subunit 3 of collagen on type IV bm

5. What does Interferon alpha and beta do? how?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

6. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
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
Anti IF
TNF alpha and IL1

7. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Immunoflourescent staining of tissue biopsies
Th cells fail to produce interferon gamma; a lot of IgE

8. What is three common causes of severe combined immunodef? What is the result of all three?
Immunoflourescent staining of tissue biopsies
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

9. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
secondary
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig

10. Which MHC presents intracellular peptides? how so?
dimer
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC I; from RER with help of the B2 microglobulin
Axillary

11. What are the cell surface proteins on NK cells?
except hyperacute
IgE
MHC I - CD16 - CD56
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

12. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
active complement pathway

13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Paracortex
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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

14. What are the major functions of Antibodies?
opsonizes
Internal iliac
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

15. What is thrombopoietin used for?
MHC I; from RER with help of the B2 microglobulin
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Thrombocytopenia
Histamine; post capillary venules - vasodilation

16. IgG...
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
opsonizes
Basophils! THey want IG E class switch!
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

17. Which HLA's are included in MHC I? MHC II?

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18. In thymic development - What is the positive selection? negative selections?
Secretory component
Anti TSh receptor
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
When you select for which MHC it will have; take out the lymphs that self react

19. describe the pathogenesis of delayed type IV hypersensitivity
S. aureus - E. Coli - aspergillus
Bind FcG for antibody dependent cellular cytotoxicity
Severe pyogenic infections early in life
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

20. Which disease is associated with DR7?
CRP - C3b - IgM
Influenza; antigenic shift; antigenic drift
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
Steroid responsive nephrotic syndrome

21. To what portion of the Antibody do the complements bind?
IgE
Barrel hoop basement membrane fenestrations
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
Fc

22. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Histamine; post capillary venules - vasodilation
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

23. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
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
Recom IL 11; thrombocytopenia
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

24. What are the three types of lymphocytes?
Yes
neutrophilia!
Type IV
B - T - and NK cells

25. What are the T cell functions?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Th2; Th1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Humoral

26. what will NK cells do to cells covered in IgG Ab? why?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Kill them because they have CD16 on them that recognize the FcG portion
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

27. What are the autoantibodies for Celiac disease?
Bind FcG for antibody dependent cellular cytotoxicity
IgG
Immunosuppression after kidney transplantation
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

28. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Anti TSh receptor
T cell activation; no with CD 4 or CD 8
pathogenesis

29. What kinds of receptors activate innate immunity?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Barrel hoop basement membrane fenestrations
TLR ad nuclear receptors
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

30. What are the main symptoms of B cell immunodeficiencies?
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
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!
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
SP infections

31. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Secretory component
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
delayed!
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

32. What is the presentation of common variable immunodef? and What are the labs?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Severe pyogenic infections early in life
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
Acts as second signal on B cells to induce class switching to IgE and IgG

33. other than C3a - what other complement acts as an anaphyloxin?
SP infections
Antimicrosomal and antithyroglobulin
Activates Th1 helper cells; Macrophages
C5a

34. What lymph node drains the duodenum - jejunum?
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 :(
Glycoproteins; HLA
Superior mesenteric
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

35. Which is the main antibody that provides passive immunity to infants?
IgG
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Basophils! THey want IG E class switch!
Thrombocytopenia

36. What is recomb alpha interferon used for?
T cell precursor
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

37. What is the pathogenesis of acute transplant rejection? When does it occur?
B - T - and NK cells
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 anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

38. which cells have more complete tolerance - B or T cells?
T
isotype
IgA
IgAs in mothers breast milk!

39. What is chronic mucocutaneous candidiasis d/t?
IgG
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
T cell dysfunction
Anti Ach receptor

40. 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
Tetanus - Botulinum - HBV - Rabies
not Ab mediated
IgM

41. A lymph node is a ________ lymphoid organ.
secondary
Tetanus - Botulinum - HBV - Rabies
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
IgM

42. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Humoral
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
Internal iliac
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

43. What is the main function of TNF alpha? How does it do this?
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Anti SS- A (anti RO) and Anti SS- B
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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

44. which antibodies prevent antigens from binding mucosal surfaces?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IgA
Cross link
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)

45. Which is the main antibody in the delayed or secondary response to an antigen?
Antihistone
Basophils! THey want IG E class switch!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgG

46. What are the autoantibodies for primary biliary cirrhosis?
...
Anti topoisomerase
Anti mitochondrial
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

47. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
cannot cross placenta
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

48. What is the main cytokine that activates eosinophils?
Activates cytotoxic CD 8 T cells as second signal
lowest concentration
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 5

49. What is serum sickness? give an example.
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
TGF beta and IL 10
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

50. What does IL 10 do? who is secreted by?
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
Internal iliac
encapsulated
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells