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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 is the main function of TNF alpha? How does it do this?
heavy chains
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
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

2. Name 5 ways Antibody diversity is generated?
Cytokine IL 10 secreted by Th2
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
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

3. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
MS
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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

4. In general What are T cells good for?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti viral and anti tumor
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Celiac

5. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
...
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
cannot cross placenta

6. What is the receptor for EBV? On what cells is that located?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cyclosporine - OKT3
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

7. In thymic development - What is the positive selection? negative selections?
A chemotactic factor for neutrophils
Glycoproteins; HLA
Paracortex
When you select for which MHC it will have; take out the lymphs that self react

8. What are the labs in brutons agammaglobulinemia?
Activates Th1 helper cells; Macrophages
neutrophilia!
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

9. 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?
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
Type IV

10. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

11. How is sirolimus different from tacrolimus?
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
Anti glutamate carboxylase and anti insulin
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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

12. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
...
IgA
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
In the germinal center of secondary follicles (In the paler center)

13. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
2 heavy chains and two light chains
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

14. Which diseases are associated with DR4?
DM type I and RA
Th2; Th1
Interferon gamma; Th1
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

15. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti Ach receptor
Thrombocytopenia

16. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IgM and IgA
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
When you select for which MHC it will have; take out the lymphs that self react
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

17. What is the most common selective Ig deficiency? What is the presentation?
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
A j chain
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

18. What is the late phase reaction of anaphylaxis allergy? what mediates it?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Negative nitroblue tetrazolium reduction test
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
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)

19. What bugs can actually infect the lymph node itself?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
DM type I and RA

20. The pathogenesis of contact dermatitis is ________ hypersensitivity
carboxy terminal
Barrel hoop basement membrane fenestrations
A recomb cytokine of IL 2; RCC and metastatic melanoma
type four

21. What are the three types of APCs?
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 :(
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Macrophages - Dendritic cells - B cells

22. What lymph node drains the testes?
Local infection/inflammation; infection of the ln itself; metastasis
Increases expression of MHC I and MHC II and also activates NK cells
Para aortic
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

23. What does granulysin do?
Immunoflourescent staining of tissue biopsies
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Cytokine IL 10 secreted by Th2
IgAs in mothers breast milk!

24. The alternative pathway is the only constutively...
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
active complement pathway
Wiskott Aldrich syndrome

25. What are the two signals required for T cells? what happens after?
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
heavy chains
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
except hyperacute

26. What is the main function of interferons?
IgM
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

27. What does IL 4 do?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Macrophages - Dendritic cells - B cells
carboxy terminal
Acts as second signal on B cells to induce class switching to IgE and IgG

28. what will NK cells do to cells covered in IgG Ab? why?
Steroid responsive nephrotic syndrome
Kill them because they have CD16 on them that recognize the FcG portion
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Edema and necrosis in that region

29. The MALT/GALT are not...
IL 4
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
encapsulated
Negative selection

30. What is the presentation of common variable immunodef? and What are the labs?
Fc
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
Anti Jo -1
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

31. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
False! B cell class switching requires a second signal

32. What lymph node drains the upper limb?
False! B cell class switching requires a second signal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Popliteal
Axillary

33. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgG

34. What are the autoantibodies for polymyositis and dermatomyositis?
Receiving preformed Antibodies
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti Jo -1

35. What do multimeric antibodies require for assembly?
A j chain
opsonizes
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

36. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
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
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 :(
Carbohydrate

37. What are the autoantibodies for drug induced lupus?
Antidote for digoxin intoxication
Cross link
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Antihistone

38. To what disease do the autoantibodies to IgG (rheumatoid factor)?
MHC II - B7
Rheumatic arthritis
opsonizes
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

39. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Basophils! THey want IG E class switch!
TGF beta and IL 10
lowest concentration

40. What lymph node drains the duodenum - jejunum?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Superior mesenteric
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

41. What are the autoantibodies for Celiac disease?
IgG
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Paracortex
C5a

42. what happens in a deficiency of C1 esterase inhibitor? DAF?
T
Hemochromatosis
Hereditary angioedema; PNH
IgAs in mothers breast milk!

43. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cyclosporine - OKT3
Anemias (esp due to renal failure)

44. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Sinusitis - otitis media - pneumonia
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

45. What are the autoantibodies for autoimmune hepatitis?
S. aureus - E. Coli - aspergillus
IgM and IgG
The patient could become cyanotic in the OR!
Anti smooth muscle

46. Which disease is associated with HLA A3?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgM and IgG
Superficial inguinal
Hemochromatosis

47. What are the cell surface proteins for Macrophages? which two are for opsonins?
NK cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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

48. Which is the main antibody in the delayed or secondary response to an antigen?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgG
T cell precursor
isotype

49. What is the most common example of passive immunity?
Humoral
A j chain
IgAs in mothers breast milk!
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

50. What are the main Cell surface proteins on T cells?
Wiskott Aldrich syndrome
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 1 and IL 6
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy