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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 are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Paracortex
Its a serine protease that activates apoptosis; NK and CD8

2. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Cross link
Anti topoisomerase
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

3. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
pale central germinal centers
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cells that stil have weird parts of their membrane that macrophages usually bite off

4. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
lowest concentration
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
DM type I and RA

5. What is the general structure of an Ab?
Immunosuppression after kidney transplantation
2 heavy chains and two light chains
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

6. What kinds of receptors activate innate immunity?
MHC class molecules bind to KIRS or CD94 to prevent killing
TLR ad nuclear receptors
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

7. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
TNF alpha and IL1
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

8. What lymph node drains the testes?
Para aortic
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

9. What do mature naive B lymphocytes express?
IgM and IgD
TNF alpha and IL1
IgG
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

10. what mediates the type II hypersensitivity? What are the two different methods?
All MHC 1/CD8
Anti topoisomerase
When you select for which MHC it will have; take out the lymphs that self react
Antibody mediated cytotoxicity; either complement dependent or complement independent

11. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Immunoflourescent staining of tissue biopsies
IL 5

12. Which disease is associated with B8?
Chronic granulomatous disease
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
Anti smooth muscle
Graves

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

14. What are the main symptoms of T cell immunodeficiencies?
Superior mesenteric
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

15. What is hereditary angioedema? What are the C3 levels?
Inferior mesenteric
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Antidesmoglein

16. What are the mediators that mast cells release?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Daclizumab; prevent ACUTE rejection of renal transplant
Immunosuppression after kidney transplantation
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

17. What lymph node drains the breast?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fc
Axillary
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

18. Name the three opsonins
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Activates Th1 helper cells; Macrophages
CRP - C3b - IgM

19. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Fc
IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

20. The ______ in the BM are DN - the DP are in the cortex of thymus
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
T cell precursor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
DM type I

21. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti Ach receptor
TGF beta and IL 10
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

22. Name two endogenous pyrogens
IL 1 and IL 6
Severe pyogenic infections early in life
Cyclosporine - OKT3
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

23. What happens in a secondary follicle?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Popliteal

24. What is the receptor for EBV? On what cells is that located?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
pathogenesis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

25. is IgM an opsonizer?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Negative!
Axillary
Complement activation (active in both)

26. Only the _______ contribute to the Fc region
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
heavy chains
Increases expression of MHC I and MHC II and also activates NK cells
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

27. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
Superficial inguinal
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)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

28. Describe complement dependent Type II hypersensitivity. Give an example.
Superficial inguinal
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
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
Liver! (they are proteins circulating in the blood)

29. Which disease is associated with DR7?
IgA
Steroid responsive nephrotic syndrome
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
TNF alpha and IL1

30. What is the marginal zone of the spleen? what happens there?
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
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
Anti SS- A (anti RO) and Anti SS- B
C5a

31. What are the autoantibodies for myasthenia gravis?
Th2; Th1
Previous transfusion; pregnant woman whose fetus had paternal antigens
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti Ach receptor

32. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 15; IL 12 - interferon Beta and interferon alpha
Sinusitis - otitis media - pneumonia
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

33. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Histamine; post capillary venules - vasodilation
Delayed type hypersensitivity

34. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Chronic granulomatous disease
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

35. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Sinusitis - otitis media - pneumonia
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

36. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Humoral
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

37. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Previous transfusion; pregnant woman whose fetus had paternal antigens
All MHC 1/CD8
pathogenesis

38. Give three examples of bacteria that use antigenic variation and how.
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Delayed type hypersensitivity
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Axillary

39. are Th cells involved in trapping of antigens of endotoxin/LPS?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
...
No because no peptide fragment!
Type IV

40. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Not thymus - BM
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

41. What are the symptoms of serum sickness?
IL 1 and IL 6
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
heavy chains
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

42. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Popliteal
Anti TSh receptor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

43. IgG...
Anti IF
Fc
lowest concentration
opsonizes

44. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
C5a
IgM and IgG
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

45. which antibody activate mast cells - basophils - and eosinophils?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Hereditary angioedema; PNH
IgE
Negative nitroblue tetrazolium reduction test

46. where are complements produced?
MHC I - CD16 - CD56
Carbohydrate
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Liver! (they are proteins circulating in the blood)

47. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
CD21 on B cells (although there is T cell lymphocytosis in EBV)
T cell activation; no with CD 4 or CD 8

48. what bacteria are a splenectomy patient most susceptible to? why?
MS - hay fever - SLE - goodpastures
Increases expression of MHC I and MHC II and also activates NK cells
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
Severe pyogenic infections early in life

49. other than C3a - what other complement acts as an anaphyloxin?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
No because no peptide fragment!
C5a
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!

50. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Viral neutralization of igM and IgG!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
The igA found in breast milk