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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. What are MHC's necessary for? By themselves?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anti U1 RNP (ribonucleoprotein)
T cell activation; no with CD 4 or CD 8
DM type I

2. What lymph node drains the duodenum - jejunum?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T 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
Superior mesenteric

3. What is thrombopoietin used for?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
TNF alpha and IL1
Thrombocytopenia
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

4. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
...

5. ________ regulate the cell mediated response.
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Humoral
active complement pathway
Lymphocytes

6. Which disease is associated with B8?
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
Paracortex
Internal iliac
Graves

7. What is the main cytokine that activates eosinophils?
No because no peptide fragment!
MHC II - B7
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 :(
IL 5

8. What is the presentation of scid? treatment?
Interferon gamma and IL 2
Its a serine protease that activates apoptosis; NK and CD8
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

9. which of the hypersensitivity reactions is not Ab mediated?
Type IV
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
Alternative splicing of mRNA
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

10. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Immunoflourescent staining of tissue biopsies
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
acute phase reactants
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

11. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
B - T - and NK cells
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cyclosporine - OKT3
Daclizumab; prevent ACUTE rejection of renal transplant

12. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
When you select for which MHC it will have; take out the lymphs that self react
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
S. aureus - E. Coli - aspergillus
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

13. The Fc region is found on the...
Interferon gamma; Th1
MHC I - CD16 - CD56
carboxy terminal
Celiac

14. What lymph node drains the lateral side of the dorsum of the foot?
Yes
Anemias (esp due to renal failure)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Popliteal

15. What are the major functions of Antibodies?
A j chain
No because no peptide fragment!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MHC II - B7

16. What is immune complex disease? give an example.
Anti IF
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Sinusitis - otitis media - pneumonia

17. What is the pathogenesis of acute transplant rejection? When does it occur?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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 are some sinopulmonary infections?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Sinusitis - otitis media - pneumonia
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

19. What lymph node drains the breast?
Axillary
Paracortex; viral infection
Tetanus - Botulinum - HBV - Rabies
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

20. What are some catalase positive organisms?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
S. aureus - E. Coli - aspergillus

21. How is the antigen loaded onto a MHC II?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IL 1 and IL 6
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

22. 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 )
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

23. What is muromonab - CD3 (OKT3)
IgG
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Hereditary angioedema; PNH
Yes

24. What is three common causes of severe combined immunodef? What is the result of all three?
Inferior mesenteric
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

25. which type of immunity is slow but long lasting? as opposed to...
Viral neutralization of igM and IgG!
Active; passive - fast but short half life (3 weeks!)
Not thymus - BM
All MHC 1/CD8

26. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
IgG
Fab portion
Humoral

27. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
encapsulated
Superficial inguinal
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

28. What is anergy? why does this occur?
IgE; by activating eosinophils
Hemochromatosis
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
dimer

29. What are the function of B cells?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

30. Which is the main antibody that provides passive immunity to infants?
IgG
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Axillary

31. What do mature naive B lymphocytes express?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Bind FcG for antibody dependent cellular cytotoxicity
carboxy terminal
IgM and IgD

32. Describe the capsular structure of a lymph node; What are the functions of the LN?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Anti glutamate carboxylase and anti insulin
neutrophilia!
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

33. What are the autoantibodies for wegeners granulomatosis?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

34. What are the main symptoms of B cell immunodeficiencies?
Histamine; post capillary venules - vasodilation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
TNF alpha and IL1
SP infections

35. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
MS - hay fever - SLE - goodpastures
The igA found in breast milk
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

36. IgG...
Carbohydrate
Stimulate the liver to release acute phase reactants
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
opsonizes

37. What is chronic mucocutaneous candidiasis d/t?
Viral neutralization of igM and IgG!
T cell dysfunction
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Activates Th1 helper cells; Macrophages

38. Which cytokines do Th2 release and For what?
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
IgG
Hemochromatosis
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

39. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
RNA segment reassortment
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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 :(

40. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Superficial inguinal
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
A chemotactic factor for neutrophils
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

41. Name the three opsonins
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Type IV
CRP - C3b - IgM

42. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Bind FcG for antibody dependent cellular cytotoxicity
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

43. Which diseases are associated with DR2?
Tetanus - Botulinum - HBV - Rabies
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
MS - hay fever - SLE - goodpastures
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

44. What is hereditary angioedema? What are the C3 levels?
In the germinal center of secondary follicles (In the paler center)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
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

45. What are the autoantibodies for primary biliary cirrhosis?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Internal iliac
Anti mitochondrial
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

46. What are the autoantibodies for pernicious anemia?
Anti IF
Basophils! THey want IG E class switch!
Superficial inguinal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

47. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
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
IgM
delayed!

48. What is oprelevkin? and What is it used for?
Edema and necrosis in that region
Recom IL 11; thrombocytopenia
Alternative splicing of mRNA
mesenchymal

49. T/F B cells do not require a second signal
TNF alpha and IL1
False! B cell class switching requires a second signal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
S. aureus - E. Coli - aspergillus

50. what cell surface marker is used for NK cells as it is unique to them?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
CD56
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
Cross link