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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.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

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 disease is associated with B8?
Th cells fail to produce interferon gamma; a lot of IgE
NK cells
Graves
Th2; Th1

2. hat is the presentation of Jobs syndrome or Hyper IgE?
Active; passive - fast but short half life (3 weeks!)
MHC II - B7
Daclizumab; prevent ACUTE rejection of renal transplant
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

3. The idiotype; the Fc portion determines the...
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Cross link
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
isotype

4. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Anti glutamate carboxylase and anti insulin
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Acts as second signal on B cells to induce class switching to IgE and IgG

5. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
IgG
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
Antidote for digoxin intoxication
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

6. What are some catalase positive organisms?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
S. aureus - E. Coli - aspergillus
dimer
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

7. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Cytokine IL 10 secreted by Th2
pathogenesis

8. What lymph node drains the thigh?
Negative selection
Superficial inguinal
Inferior mesenteric
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

9. can igG cross the placenta?
Not thymus - BM
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
Yes
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

10. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
mesenchymal
Graves

11. What is Aldesleukin? What is it used for
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
Antidote for digoxin intoxication
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anti IF

12. What are target cells?
Carbohydrate
Hereditary angioedema; PNH
Cells that stil have weird parts of their membrane that macrophages usually bite off
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

13. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
MHC I - CD16 - CD56

14. what prevents NK cells from killing normal cells if their default is to kill?
Celiac
except hyperacute
MHC class molecules bind to KIRS or CD94 to prevent killing
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

15. What are the main Cell surface proteins on T cells?
Anti Ach receptor
Lymphocytes
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
No because no peptide fragment!

16. What is the defect in hyper IgM syndrome? What are the lab results?
The patient could become cyanotic in the OR!
Pernicious Anemia and Hashimotos
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

17. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
SP infections
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
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
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

18. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
IgM
Histamine; post capillary venules - vasodilation
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

19. which antibody activate mast cells - basophils - and eosinophils?
Basophils! THey want IG E class switch!
lowest concentration
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
IgE

20. What is the common variable immunodeficiency ? How is it different from Brutons?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
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

21. What is the autoantibody for SLE that is nonspecific? Specific?
Anti Ach receptor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

22. What are the autoantibodies for systemic sclerosis?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti topoisomerase
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

23. The ______ in the BM are DN - the DP are in the cortex of thymus
isotype
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
T cell precursor

24. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
S. aureus - E. Coli - aspergillus
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

25. What is three common causes of severe combined immunodef? What is the result of all three?
MS
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
dimer
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

26. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Negative nitroblue tetrazolium reduction test
MS
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

27. Which antibody mediates immunity to worms? how?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgE; by activating eosinophils
Axillary

28. is IgM an opsonizer?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anti viral and anti tumor
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Negative!

29. The lymphocytes are ________ origin
Yes
Activate macrophages
Increases expression of MHC I and MHC II and also activates NK cells
mesenchymal

30. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Chronic granulomatous disease

31. __________ are a part of the innate system.
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Complement activation (active in both)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
NK cells

32. Which cytokines do Th2 release and For what?
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
Fab portion
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
TGF beta and IL 10

33. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Sinusitis - otitis media - pneumonia
pathogenesis

34. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IgG

35. What are the autoantibodies for type I diabetes mellitus?
T
Anti glutamate carboxylase and anti insulin
Anti IF
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

36. What is the main function of interferons?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

37. Which MHC presents intracellular peptides? how so?
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
T cell dysfunction
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
MHC I; from RER with help of the B2 microglobulin

38. What are the PALS?
T cell precursor
MHC II - B7
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Interferon gamma; Th1

39. What cytokines are released by Th1 cells?
Anti mitochondrial
neutrophilia!
Interferon gamma and IL 2
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

40. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Its main effect is a defect in Ab opsonization for killing

41. Type Iv hypersensitivity is...
IgE; by activating eosinophils
A - B - C; all the D's
delayed!
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 :(

42. Which are the only two antiinflammatory cytokines?
IgM and IgA
Paracortex
TGF beta and IL 10
DM type I

43. what secretes IL 4?
Anti mitochondrial
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Basophils! THey want IG E class switch!

44. The Fc region is found on the...
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
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
Anti Ach receptor
carboxy terminal

45. Which antibodies can be multimeric?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
pale central germinal centers
Cytokine IL 10 secreted by Th2
IgM and IgA

46. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
pathogenesis
Paracortex; viral infection
False! B cell class switching requires a second signal
Anti viral and anti tumor

47. What are howell jolly bodies?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

48. Only the _______ contribute to the Fc region
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Negative selection
heavy chains

49. Complements are...
acute phase reactants
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Inferior mesenteric
Anemias (esp due to renal failure)

50. 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?
Antimicrosomal and antithyroglobulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
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