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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 clinical use for azathioprine?
...
Not thymus - BM
By transcytosis
Glycoproteins; HLA

2. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
C5a
IgE
neutrophilia!

3. What is the defect in hyper IgM syndrome? What are the lab results?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Influenza; antigenic shift; antigenic drift
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

4. What are the cell surface proteins for Macrophages? which two are for opsonins?
Cyclosporine - OKT3
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Liver! (they are proteins circulating in the blood)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

5. In general What are T cells good for?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti viral and anti tumor
Remove encapsulated bacateria
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

6. What are target cells?
MHC I - CD16 - CD56
Cells that stil have weird parts of their membrane that macrophages usually bite off
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Carbohydrate

7. What cytokines to Th2 secrete?
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
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
IL 4 - 5 - 10 - 6
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

8. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti TSh receptor
Daclizumab; prevent ACUTE rejection of renal transplant
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

9. The MALT/GALT are not...
Complement activation (active in both)
The igA found in breast milk
encapsulated
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

10. What is the main cytokine released by T cells? What does it do
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Paracortex; viral infection
Immunosuppression after kidney transplantation
IL 3; supports growth and differentiation of bone marrow stem cells

11. 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
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
Internal iliac

12. What is the toxicity of muromonab?
Type IV
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Severe pyogenic infections early in life
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

13. What is the main cytokine that activates eosinophils?
IL 5
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

14. What is the mechanism for sirolimus? what else it known as?
No because no peptide fragment!
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
secondary

15. What lymph node drains the upper limb?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Axillary

16. What is recomb gamma interferon used for?
Chronic granulomatous disease
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Daclizumab; prevent ACUTE rejection of renal transplant
DM type I and RA

17. What are four results of a splenectomy?
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)
Basophils! THey want IG E class switch!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

18. can igG cross the placenta?
IgE; by activating eosinophils
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Immunoflourescent staining of tissue biopsies
Yes

19. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Stimulate the liver to release acute phase reactants
Fab portion
Delayed type hypersensitivity

20. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
SP infections
Antibody mediated cytotoxicity; either complement dependent or complement independent
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

21. What do mature naive B lymphocytes express?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
When you select for which MHC it will have; take out the lymphs that self react
IgM and IgD

22. 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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Acts as second signal on B cells to induce class switching to IgE and IgG
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

23. What are the main symptoms of B cell immunodeficiencies?
If there is class switching and plasma cell production (that is when memory cells are produced)
SP infections
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Antidesmoglein

24. What are the autoantibodies for Celiac disease?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lymphocytes

25. What happens in a deficiency of C3?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

26. What is the pathology of acute transplant rejection? is it reversible?
lowest concentration
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

27. 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antimicrosomal and antithyroglobulin
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

28. what cytokine does basophils secrete?
Cyclosporine - OKT3
IL 4
cannot cross placenta
Severe pyogenic infections early in life

29. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Delayed type hypersensitivity
Th2; Th1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

30. IgE has the ___________ in the serum
Internal iliac
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
lowest concentration
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

31. What is recomb alpha interferon used for?
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!
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

32. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgE; by activating eosinophils

33. which cells have more complete tolerance - B or T cells?
Inferior mesenteric
pentamer
T
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

34. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgG
Anti Ach receptor
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

35. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Fab portion
Rheumatic arthritis

36. What lymph node drains the breast?
Anti glutamate carboxylase and anti insulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Axillary
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

37. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
cannot cross placenta
except hyperacute
Macrophages - Dendritic cells - B cells
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

38. What is epo used for?
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
Anemias (esp due to renal failure)
Secretory component
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

39. What are superantigens? give two examples.
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Popliteal
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
Graves

40. The Fc region is found on the...
neutrophilia!
NK cells
carboxy terminal
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

41. are Th cells involved in trapping of antigens of endotoxin/LPS?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Bind FcG for antibody dependent cellular cytotoxicity
Steroid responsive nephrotic syndrome
No because no peptide fragment!

42. give an example of how influenza does a major antigenic shift.
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Cells that stil have weird parts of their membrane that macrophages usually bite off
RNA segment reassortment
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

43. How do you test for type III hypersensitivity?
Anemias (esp due to renal failure)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Immunoflourescent staining of tissue biopsies
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

44. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
Hemochromatosis
T cell dysfunction

45. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
S. aureus - E. Coli - aspergillus
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Th2; Th1

46. How is sirolimus different from tacrolimus?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
SP infections
Rheumatic arthritis

47. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
pentamer
Liver! (they are proteins circulating in the blood)
Hereditary angioedema; PNH
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

48. What are the main symptoms of T cell immunodeficiencies?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Activates Th1 helper cells; Macrophages
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

49. Which diseases are associated with DR4?
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
DM type I and RA
Anti TSh receptor
Complement activation (active in both)

50. What does IL 4 do?
Cross link
neutrophilia!
Acts as second signal on B cells to induce class switching to IgE and IgG
cannot cross placenta