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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 is the main antibody that provides passive immunity to infants?
Negative selection
IgG
Hemochromatosis
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

2. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Not thymus - BM
The patient could become cyanotic in the OR!
Rheumatic arthritis
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

3. What is the pathology of acute transplant rejection? is it reversible?
Acts as second signal on B cells to induce class switching to IgE and IgG
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

4. What links the adaptive and innate immunity?
Cytokine IL 10 secreted by Th2
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Complement activation (active in both)
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

5. what mediates the type II hypersensitivity? What are the two different methods?
Antidote for digoxin intoxication
Celiac
Antibody mediated cytotoxicity; either complement dependent or complement independent
CRP - C3b - IgM

6. Which type of selection of thymic development provides central tolerance?
dimer
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Negative selection
MS - hay fever - SLE - goodpastures

7. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Humoral
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

8. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
MHC II - B7
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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

9. 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 )
Internal iliac
acute phase reactants
secondary

10. What are the two signals to kill for NK cells?
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
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

11. What are the function of B cells?
Sinusitis - otitis media - pneumonia
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

12. IgE has the ___________ in the serum
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!
lowest concentration
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

13. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
A recomb cytokine of IL 2; RCC and metastatic melanoma
Active; passive - fast but short half life (3 weeks!)

14. Which is the main antibody in the delayed or secondary response to an antigen?
IL 1 and IL 6
IgG
Anti viral and anti tumor
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

15. What is anergy? why does this occur?
TGF beta and IL 10
IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Activates cytotoxic CD 8 T cells as second signal

16. What is the white pulp of the spleen?
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 :(
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Anti Jo -1

17. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Yes
A recomb cytokine of IL 2; RCC and metastatic melanoma
carboxy terminal

18. How fast does it occur?
The patient could become cyanotic in the OR!
Negative nitroblue tetrazolium reduction test
IL 4 - 5 - 10 - 6
Interferon gamma; Th1

19. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
CRP - C3b - IgM
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!
The igA found in breast milk
lowest concentration

20. What are four results of a splenectomy?
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
Severe pyogenic infections early in life
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Basophils! THey want IG E class switch!

21. What is muromonab - CD3 (OKT3)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

22. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Sinusitis - otitis media - pneumonia
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Th cells fail to produce interferon gamma; a lot of IgE
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

23. what prevents NK cells from killing normal cells if their default is to kill?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MHC class molecules bind to KIRS or CD94 to prevent killing
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

24. What is passive immunity?
encapsulated
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
Receiving preformed Antibodies
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

25. What are the three types of lymphocytes?
B - T - and NK cells
Lymphocytes
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Interferon gamma; Th1

26. From where do cytokines come from?
Fab portion
Its a serine protease that activates apoptosis; NK and CD8
Secretory component
Lymphocytes

27. What is the pathogenesis of a candida skin test?
Anemias (esp due to renal failure)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Delayed type hypersensitivity
pathogenesis

28. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Acts as second signal on B cells to induce class switching to IgE and IgG
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

29. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Popliteal
CRP - C3b - IgM
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

30. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Celiac
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

31. What is the general structure of an Ab?
2 heavy chains and two light chains
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
MHC II - B7
RNA segment reassortment

32. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
T cell precursor
IgE
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

33. What are the autoantibodies for systemic sclerosis?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
except hyperacute
Anti topoisomerase
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

34. What lymph node drains the upper limb?
IgG
MS - hay fever - SLE - goodpastures
Axillary
Secretory component

35. What is recomb beta interferon used for?
IgM and IgG
MS
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
Humoral

36. What is the most common example of passive immunity?
carboxy terminal
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgAs in mothers breast milk!
T cell activation; no with CD 4 or CD 8

37. What is the clinical use of Muromonab?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Immunosuppression after kidney transplantation
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
Barrel hoop basement membrane fenestrations

38. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Its main effect is a defect in Ab opsonization for killing
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

39. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Glycoproteins; HLA
S. aureus - E. Coli - aspergillus
T cell activation; no with CD 4 or CD 8
Paracortex

40. what ensure that a memory response is generated?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
If there is class switching and plasma cell production (that is when memory cells are produced)
Receiving preformed Antibodies
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

41. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
Graves
S. aureus - E. Coli - aspergillus
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

42. What are the main Cell surface proteins on T cells?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Daclizumab; prevent ACUTE rejection of renal transplant
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

43. What is the main function of IL 8?
A - B - C; all the D's
delayed!
Cells that stil have weird parts of their membrane that macrophages usually bite off
A chemotactic factor for neutrophils

44. ________ regulate the cell mediated response.
Humoral
Secretory component
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 :(
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

45. which cells have more complete tolerance - B or T cells?
Fc
T
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

46. which B and T cell disorder presents with specifically low IgM?
Superficial inguinal
Negative!
acute phase reactants
Wiskott Aldrich syndrome

47. which antibody activate mast cells - basophils - and eosinophils?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IgE
Liver! (they are proteins circulating in the blood)
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

48. To what portion of the Antibody do the complements bind?
Fc
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
except hyperacute
IgAs in mothers breast milk!

49. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Antidote for digoxin intoxication
Cross link
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

50. describe the pathogenesis of delayed type IV hypersensitivity
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Barrel hoop basement membrane fenestrations
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
T cells react to the angtigen and activate leukocyted (macrophage acitivation)