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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. What is three common causes of severe combined immunodef? What is the result of all three?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Negative!
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

2. What does IL 5 do?
dimer
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
A chemotactic factor for neutrophils

3. other than eat and bite RBCs what else do Macrophages of spleen do>
not Ab mediated
Remove encapsulated bacateria
SP infections
Anti glutamate carboxylase and anti insulin

4. What do multimeric antibodies require for assembly?
A j chain
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
pentamer
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

5. In thymic development - What is the positive selection? negative selections?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
When you select for which MHC it will have; take out the lymphs that self react
RNA segment reassortment
MHC II - B7

6. what secretes IL 4?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Superficial inguinal
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
Basophils! THey want IG E class switch!

7. Only the _______ contribute to the Fc region
Antihistone
Negative nitroblue tetrazolium reduction test
Cytokine IL 10 secreted by Th2
heavy chains

8. What lymph node drains the sigmoid colon?
Inferior mesenteric
IgM and IgD
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti smooth muscle

9. IgM can exist as a _______ also
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
pentamer
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
...

10. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
T cell dysfunction

11. Which antibody mediates immunity to worms? how?
If there is class switching and plasma cell production (that is when memory cells are produced)
IgE; by activating eosinophils
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

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

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13. What are the autoantibodies for graves?
Bind FcG for antibody dependent cellular cytotoxicity
DM type I and RA
Anti TSh receptor
Fc

14. What links the adaptive and innate immunity?
In the germinal center of secondary follicles (In the paler center)
Bind FcG for antibody dependent cellular cytotoxicity
Complement activation (active in both)
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

15. describe the pathogenesis of delayed type IV hypersensitivity
Hereditary angioedema; PNH
Anti TSh receptor
Interferon gamma; Th1
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

16. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Antibody mediated cytotoxicity; either complement dependent or complement independent
pathogenesis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

17. What are some sinopulmonary infections?
secondary
Increases expression of MHC I and MHC II and also activates NK cells
Sinusitis - otitis media - pneumonia
2 heavy chains and two light chains

18. What does CD16 on NK cells do?
RNA segment reassortment
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Bind FcG for antibody dependent cellular cytotoxicity

19. For which toxins are preformed antibodies (passive) given?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti SS- A (anti RO) and Anti SS- B
Tetanus - Botulinum - HBV - Rabies

20. what prevents NK cells from killing normal cells if their default is to kill?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
MHC class molecules bind to KIRS or CD94 to prevent killing
Cross link

21. What is the toxicity of azathioprine?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
...
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Superficial inguinal

22. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Complement activation (active in both)

23. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
CRP - C3b - IgM
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

24. which antibodies can bind complement?
Hereditary angioedema; PNH
IgM and IgG
lowest concentration
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

25. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
T
...
TNF alpha and IL1

26. What lymph node drains the scrotum?
Superficial inguinal
RNA segment reassortment
B - T - and NK cells
MHC I; from RER with help of the B2 microglobulin

27. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
not Ab mediated
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Severe pyogenic infections early in life

28. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Yes
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
False! B cell class switching requires a second signal
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

29. What kinds of receptors activate innate immunity?
Anti topoisomerase
IL 15; IL 12 - interferon Beta and interferon alpha
TLR ad nuclear receptors
C5a

30. What is serum sickness? give an example.
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

31. What can cause a lymph node enlargement?
...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Local infection/inflammation; infection of the ln itself; metastasis
Severe pyogenic infections early in life

32. What are the PALS?
Humoral
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

33. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Bind FcG for antibody dependent cellular cytotoxicity
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

34. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
No because no peptide fragment!
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
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

35. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IL 4 - 5 - 10 - 6
CD21 on B cells (although there is T cell lymphocytosis in EBV)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

36. What is the mechanism for sirolimus? what else it known as?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Anti Ach receptor
Delayed type hypersensitivity

37. 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
Bind FcG for antibody dependent cellular cytotoxicity
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

38. How is i Th1 helper cell inhibited?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
Cytokine IL 10 secreted by Th2
A - B - C; all the D's

39. What is the main cytokine that activates eosinophils?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC I; from RER with help of the B2 microglobulin
IL 5

40. __________ are a part of the innate system.
Anti mitochondrial
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
NK cells
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

41. T/F B cells do not require a second signal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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
Remove encapsulated bacateria
False! B cell class switching requires a second signal

42. what characterizes an arthus reaction?
Edema and necrosis in that region
NK cells
IL 3; supports growth and differentiation of bone marrow stem cells
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

43. What is the marginal zone of the spleen? what happens there?
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
Steroid responsive nephrotic syndrome
dimer
Immunoflourescent staining of tissue biopsies

44. which cells have more complete tolerance - B or T cells?
pathogenesis
T
In the germinal center of secondary follicles (In the paler center)
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

45. Which disease is associated with DR3?
DM type I
Local infection/inflammation; infection of the ln itself; metastasis
T cell precursor
IgE

46. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Daclizumab; prevent ACUTE rejection of renal transplant
cannot cross placenta
Anti glutamate carboxylase and anti insulin

47. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Cells that stil have weird parts of their membrane that macrophages usually bite off
delayed!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

48. What is the toxicity of muromonab?
Negative!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Daclizumab; prevent ACUTE rejection of renal transplant
Cyclosporine - OKT3

49. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
MHC I - CD16 - CD56
Glycoproteins; HLA
Activates Th1 helper cells; Macrophages

50. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Type IV