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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 immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Internal iliac

2. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Fab portion
Cells that stil have weird parts of their membrane that macrophages usually bite off
Th cells fail to produce interferon gamma; a lot of IgE

3. 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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

4. what cell surface proteins are on all APCs?
Superior mesenteric
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
MHC II - B7

5. which type of immunity is slow but long lasting? as opposed to...
Its a serine protease that activates apoptosis; NK and CD8
C5a
Basophils! THey want IG E class switch!
Active; passive - fast but short half life (3 weeks!)

6. How fast does it occur?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Bind FcG for antibody dependent cellular cytotoxicity
The patient could become cyanotic in the OR!
Anti TSh receptor

7. __________ are a part of the innate system.
IgM
NK cells
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

8. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
Increases expression of MHC I and MHC II and also activates NK cells
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
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

9. What is an example of a parasite showing antigenic variation?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Activate macrophages
The igA found in breast milk

10. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Internal iliac
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

11. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
active complement pathway
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

12. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Pernicious Anemia and Hashimotos
neutrophilia!
Cells that stil have weird parts of their membrane that macrophages usually bite off
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

13. Name the three opsonins
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
CRP - C3b - IgM
IgG

14. What are the autoantibodies for hashimotos?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antimicrosomal and antithyroglobulin
Recom IL 11; thrombocytopenia
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

15. other than C3a - what other complement acts as an anaphyloxin?
Macrophages - Dendritic cells - B cells
C5a
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

16. What are the autoantibodies for wegeners granulomatosis?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
RNA segment reassortment
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Yes

17. what cell surface marker is used for NK cells as it is unique to them?
CD56
Anti TSh receptor
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

18. What are four results of a splenectomy?
Antidote for digoxin intoxication
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

19. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
MS
Sinusitis - otitis media - pneumonia
not Ab mediated

20. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
MS
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

21. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgE
pale central germinal centers
Pernicious Anemia and Hashimotos

22. How do you test for chronic granulomatous disease?
Lymphocytes
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
MHC I; from RER with help of the B2 microglobulin
Negative nitroblue tetrazolium reduction test

23. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
IL 3; supports growth and differentiation of bone marrow stem cells
Histamine; post capillary venules - vasodilation
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti U1 RNP (ribonucleoprotein)

24. The pathogenesis of contact dermatitis is ________ hypersensitivity
Complement activation (active in both)
mesenchymal
type four
IgM

25. What is serum sickness? give an example.
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
Inferior mesenteric
acute phase reactants
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

26. What is hereditary angioedema? What are the C3 levels?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Kill them because they have CD16 on them that recognize the FcG portion
Remove encapsulated bacateria
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

27. What are the autoantibodies for sjorgens syndrome?
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
Anti SS- A (anti RO) and Anti SS- B
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Receiving preformed Antibodies

28. 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?
carboxy terminal
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
TNF alpha and IL1

29. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti glutamate carboxylase and anti insulin
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

30. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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)
Anti SS- A (anti RO) and Anti SS- B
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Alternative splicing of mRNA

31. what bacteria are a splenectomy patient most susceptible to? why?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Lymphocytes
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 :(

32. What is Aldesleukin? What is it used for
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IgG
T cell dysfunction
A recomb cytokine of IL 2; RCC and metastatic melanoma

33. What are the autoantibodies for Mixed connective tissue disease?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti U1 RNP (ribonucleoprotein)

34. For which toxins are preformed antibodies (passive) given?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Tetanus - Botulinum - HBV - Rabies
Increases expression of MHC I and MHC II and also activates NK cells

35. What is the pathogenesis of a candida skin test?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Negative!
Delayed type hypersensitivity

36. IgM can fix complement but...
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Thrombocytopenia
cannot cross placenta

37. IgG...
Local infection/inflammation; infection of the ln itself; metastasis
opsonizes
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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

38. What lymph node drains the breast?
Macrophages - Dendritic cells - B cells
Axillary
Anti Jo -1
Paracortex; viral infection

39. What does IL 5 do?
No because no peptide fragment!
Immunosuppression after kidney transplantation
Yes
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

40. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgM

41. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
Fc
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgE; by activating eosinophils

42. What is recomb gamma interferon used for?
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
Chronic granulomatous disease
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
Anti U1 RNP (ribonucleoprotein)

43. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Anti TSh receptor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

44. What is the main function of interferons?
pathogenesis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
pentamer

45. IgE has the ___________ in the serum
lowest concentration
IgAs in mothers breast milk!
Local infection/inflammation; infection of the ln itself; metastasis
In the germinal center of secondary follicles (In the paler center)

46. How do you test for type III hypersensitivity?
Interferon gamma and IL 2
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Immunoflourescent staining of tissue biopsies
Kill them because they have CD16 on them that recognize the FcG portion

47. Describe the Mannose Lectin pathway
not Ab mediated
Complement activation (active in both)
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

48. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Cross link
mesenchymal

49. which antibodies prevent antigens from binding mucosal surfaces?
Negative!
T
IgA
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

50. What are the two signals required for Th1 cells? what happens after then activated?
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
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!