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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. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Negative nitroblue tetrazolium reduction test
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

2. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Type IV
opsonizes
Anemias (esp due to renal failure)
Alternative splicing of mRNA

3. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IL 15; IL 12 - interferon Beta and interferon alpha
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
Severe pyogenic infections early in life
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

4. Which is the most abundant antibody in blood?
IgG
acute phase reactants
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Remove encapsulated bacateria

5. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
T cell dysfunction
except hyperacute

6. What does IgA pick up from epithelial cells before being secreted?
Secretory component
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Humoral
Severe pyogenic infections early in life

7. What are the mediators that mast cells release?
Cross link
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

8. 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 )
opsonizes
isotype
Cyclosporine - OKT3

9. What lymph node drains the rectum (above the pectinate line)?
By transcytosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
A - B - C; all the D's
Internal iliac

10. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
Severe pyogenic infections early in life
Increases expression of MHC I and MHC II and also activates NK cells
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

11. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
A j chain
Cyclosporine - OKT3
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

12. Which diseases are associated with DR5?
neutrophilia!
Pernicious Anemia and Hashimotos
Viral neutralization of igM and IgG!
IL 1 and IL 6

13. Which cytokines do Th2 release and For what?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Complement activation (active in both)
not Ab mediated
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

14. Which disease is associated with B8?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Graves
pale central germinal centers
IL 5

15. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
CD56
Steroid responsive nephrotic syndrome

16. How does complement link innate and adaptive?
opsonizes
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

17. other than mediating shock - what else does TNF alpha do? who releases it mainly?
DM type I
Activates Th1 helper cells; Macrophages
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Remove encapsulated bacateria

18. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
heavy chains
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
IgAs in mothers breast milk!

19. which of the hypersensitivity reactions is not Ab mediated?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Type IV
Sinusitis - otitis media - pneumonia
Cells that stil have weird parts of their membrane that macrophages usually bite off

20. What is the clinical use for azathioprine?
2 heavy chains and two light chains
...
By transcytosis
CRP - C3b - IgM

21. What cytokines to Th2 secrete?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IL 4 - 5 - 10 - 6
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
MHC class molecules bind to KIRS or CD94 to prevent killing

22. What is hereditary angioedema? What are the C3 levels?
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
IgE
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

23. The lymphocytes are ________ origin
MHC II - B7
mesenchymal
Anti viral and anti tumor
Pernicious Anemia and Hashimotos

24. What is the toxicity of muromonab?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Celiac
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC I; from RER with help of the B2 microglobulin

25. What lymph node drains the stomach?
Celiac
Fc
Rheumatic arthritis
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

26. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

27. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Its main effect is a defect in Ab opsonization for killing
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Antibody mediated cytotoxicity; either complement dependent or complement independent

28. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
IL 15; IL 12 - interferon Beta and interferon alpha
Histamine; post capillary venules - vasodilation
IgA
type four

29. The MALT/GALT are not...
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Fc
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
encapsulated

30. 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
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
Thrombocytopenia
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

31. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Increases expression of MHC I and MHC II and also activates NK cells
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
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
Paracortex; viral infection

32. IgM can fix complement but...
By transcytosis
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Local infection/inflammation; infection of the ln itself; metastasis
cannot cross placenta

33. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
MHC I; from RER with help of the B2 microglobulin
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

34. What does IL 4 do?
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
2 heavy chains and two light chains
IgA

35. What is the defect in hyper IgM syndrome? What are the lab results?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Liver! (they are proteins circulating in the blood)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

36. So antibodies are the effectors for the humoral response. List some of their functions.
Influenza; antigenic shift; antigenic drift
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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

37. Which is the main antibody that provides passive immunity to infants?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Active; passive - fast but short half life (3 weeks!)
IgG
Anti TSh receptor

38. Other than stimulating fever - what else does IL 6 do?
A recomb cytokine of IL 2; RCC and metastatic melanoma
IgM and IgD
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Stimulate the liver to release acute phase reactants

39. other than eat and bite RBCs what else do Macrophages of spleen do>
When you select for which MHC it will have; take out the lymphs that self react
Remove encapsulated bacateria
Anti IF
MS

40. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Antidesmoglein
Activate macrophages
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

41. What is the pathogenesis of a candida skin test?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti Jo -1
Delayed type hypersensitivity
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

42. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
The igA found in breast milk
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
except hyperacute
Influenza; antigenic shift; antigenic drift

43. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Acts as second signal on B cells to induce class switching to IgE and IgG
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

44. What is the presentation of Brutons agammaglobulinemia?
Influenza; antigenic shift; antigenic drift
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Stimulate the liver to release acute phase reactants

45. What are the symptoms of serum sickness?
Anemias (esp due to renal failure)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IgM and IgG

46. What type of side chains are found on Fc region of an antibody?
Th cells fail to produce interferon gamma; a lot of IgE
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 5
Carbohydrate

47. What is the most common selective Ig deficiency? What is the presentation?
Humoral
Superficial inguinal
NK cells
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

48. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Fab portion
Rheumatic arthritis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

49. What are the two signals required for T cells? what happens after?
TNF alpha and IL1
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
DM type I
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

50. What do mature naive B lymphocytes express?
IgM and IgD
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgG
Activate macrophages