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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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Match each statement with the correct term.
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1. 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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Basophils! THey want IG E class switch!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

2. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
pathogenesis
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Axillary
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

3. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

4. can igG cross the placenta?
Yes
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
SP infections
Type IV

5. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Anti topoisomerase
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

6. What is anergy? why does this occur?
Barrel hoop basement membrane fenestrations
IL 4
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

7. What is serum sickness? give an example.
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Steroid responsive nephrotic syndrome
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

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

9. What is the autoantibody for SLE that is nonspecific? Specific?
MHC I - CD16 - CD56
Antidote for digoxin intoxication
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

10. What is chronic mucocutaneous candidiasis d/t?
2 heavy chains and two light chains
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
T cell dysfunction
opsonizes

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

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12. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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)
Fab portion

13. What is the receptor for EBV? On what cells is that located?
secondary
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
neutrophilia!

14. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Alternative splicing of mRNA
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Activate macrophages

15. What can cause a lymph node enlargement?
MHC I - CD16 - CD56
Local infection/inflammation; infection of the ln itself; metastasis
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Stimulate the liver to release acute phase reactants

16. Which diseases are associated with DR4?
Immunoflourescent staining of tissue biopsies
DM type I and RA
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgAs in mothers breast milk!

17. What are the autoantibodies for primary biliary cirrhosis?
Liver! (they are proteins circulating in the blood)
Its main effect is a defect in Ab opsonization for killing
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti mitochondrial

18. What are the cell surface proteins on NK cells?
NK cells
Viral neutralization of igM and IgG!
MHC I - CD16 - CD56
Lymphocytes

19. What cytokines are released by Th1 cells?
Influenza; antigenic shift; antigenic drift
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Paracortex
Interferon gamma and IL 2

20. where do NK cells develop?
Not thymus - BM
Cross link
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

21. What are the autoantibodies for drug induced lupus?
A j chain
MS - hay fever - SLE - goodpastures
Antihistone
Anti viral and anti tumor

22. What are the autoantibodies for graves?
Anti TSh receptor
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
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
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

23. 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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

24. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
T cell activation; no with CD 4 or CD 8
Alternative splicing of mRNA
Hemochromatosis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

25. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Acts as second signal on B cells to induce class switching to IgE and IgG

26. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

27. Which disease is associated with B8?
A - B - C; all the D's
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Graves
NK cells

28. Which is the main antibody that provides passive immunity to infants?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgG
Yes
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

29. What lymph node drains the sigmoid colon?
carboxy terminal
Sinusitis - otitis media - pneumonia
Inferior mesenteric
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

30. What does Interferon alpha and beta do? how?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

31. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Glycoproteins; HLA

32. IgE has the ___________ in the serum
Inferior mesenteric
lowest concentration
Steroid responsive nephrotic syndrome
Hemochromatosis

33. Type Iv hypersensitivity is...
Previous transfusion; pregnant woman whose fetus had paternal antigens
Type IV
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
delayed!

34. Name two endogenous pyrogens
IL 1 and IL 6
Fc
Glycoproteins; HLA
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

35. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Superficial inguinal
A j chain
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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

36. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Th2; Th1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Cytokine IL 10 secreted by Th2

37. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Carbohydrate
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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

38. What is the clinical use for sirolimus? what should you combine it with?
Viral neutralization of igM and IgG!
2 heavy chains and two light chains
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Basophils! THey want IG E class switch!

39. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Antihistone
MS - hay fever - SLE - goodpastures

40. What is the general structure of an Ab?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Recom IL 11; thrombocytopenia
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
2 heavy chains and two light chains

41. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Complement activation (active in both)
Tetanus - Botulinum - HBV - Rabies
2 heavy chains and two light chains

42. Give three examples of bacteria that use antigenic variation and how.
NK cells
Axillary
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

43. which antibodies can bind complement?
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
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
Activates cytotoxic CD 8 T cells as second signal
IgM and IgG

44. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

45. Name the three opsonins
CRP - C3b - IgM
Cyclosporine - OKT3
except hyperacute
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

46. What are superantigens? give two examples.
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
Paracortex
IgE; by activating eosinophils
Popliteal

47. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Its main effect is a defect in Ab opsonization for killing
DM type I and RA
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
Activates cytotoxic CD 8 T cells as second signal

48. What does granulysin do?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Popliteal
pathogenesis
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

49. What is the white pulp of the spleen?
Axillary
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
carboxy terminal

50. What do multimeric antibodies require for assembly?
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
A j chain
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

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USMLE Step 1 Immunology

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