Test your basic knowledge |

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. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Interferon gamma and IL 2
If there is class switching and plasma cell production (that is when memory cells are produced)
DM type I and RA

2. Which diseases are associated with DR4?
DM type I and RA
Pernicious Anemia and Hashimotos
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
dimer

3. What are some catalase positive organisms?
Paracortex
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
S. aureus - E. Coli - aspergillus
Celiac

4. What are the main Cell surface proteins on T cells?
Negative!
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
type four

5. Monomer in circulation - ___ when secreted
Anti viral and anti tumor
A chemotactic factor for neutrophils
dimer
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

6. What are the main symptoms of B cell immunodeficiencies?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Cytokine IL 10 secreted by Th2
SP infections
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

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

Warning: Invalid argument supplied for foreach() in /var/www/html/basicversity.com/show_quiz.php on line 183

8. What are the major functions of Antibodies?
Interferon gamma; Th1
Anti TSh receptor
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

9. What is oprelevkin? and What is it used for?
Stimulate the liver to release acute phase reactants
Basophils! THey want IG E class switch!
Delayed type hypersensitivity
Recom IL 11; thrombocytopenia

10. What is colostrum?
Humoral
The igA found in breast milk
Negative selection
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

11. What are C1 - C2 - C3 - C4 important for?
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
IgE
Anti viral and anti tumor
Viral neutralization of igM and IgG!

12. What are the T cell functions?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
isotype

13. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Cells that stil have weird parts of their membrane that macrophages usually bite off
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

14. What are the autoantibodies for hashimotos?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Antimicrosomal and antithyroglobulin
2 heavy chains and two light chains

15. How is i Th1 helper cell inhibited?
Not thymus - BM
Tetanus - Botulinum - HBV - Rabies
Cytokine IL 10 secreted by Th2
Superficial inguinal

16. What are the autoantibodies for primary biliary cirrhosis?
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti mitochondrial
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

17. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Bind FcG for antibody dependent cellular cytotoxicity
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

18. Which are the only two antiinflammatory cytokines?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Glycoproteins; HLA
Humoral
TGF beta and IL 10

19. What is the defect in hyper IgM syndrome? What are the lab results?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
pathogenesis
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

20. Which antibodies can be multimeric?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Superior mesenteric
S. aureus - E. Coli - aspergillus
IgM and IgA

21. What lymph node drains the testes?
MHC class molecules bind to KIRS or CD94 to prevent killing
Para aortic
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Tetanus - Botulinum - HBV - Rabies

22. what cell surface proteins are on all APCs?
pathogenesis
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
MHC II - B7
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

23. other than eat and bite RBCs what else do Macrophages of spleen do>
C5a
Remove encapsulated bacateria
Axillary
Alternative splicing of mRNA

24. What are the autoantibodies for wegeners granulomatosis?
Anti Jo -1
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

25. Which disease is associated withB B27?
In the germinal center of secondary follicles (In the paler center)
acute phase reactants
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti U1 RNP (ribonucleoprotein)

26. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IgM
Graves
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia

27. What is an example of a parasite showing antigenic variation?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Not thymus - BM

28. What is passive immunity?
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgG
Receiving preformed Antibodies

29. What are the mediators that mast cells release?
Activates Th1 helper cells; Macrophages
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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

30. Which antibody mediates immunity to worms? how?
IL 5
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Liver! (they are proteins circulating in the blood)
IgE; by activating eosinophils

31. What is the clinical use for sirolimus? what should you combine it with?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Superficial inguinal
Daclizumab; prevent ACUTE rejection of renal transplant
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

32. Other than stimulating fever - what else does IL 6 do?
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Stimulate the liver to release acute phase reactants

33. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IL 4 - 5 - 10 - 6

34. What is the pathology in hyperacute transplant rejection?
Negative selection
not Ab mediated
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC II - B7

35. What are target cells?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
MHC I - CD16 - CD56

36. What are the autoantibodies for Celiac disease?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Negative nitroblue tetrazolium reduction test
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

37. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
False! B cell class switching requires a second signal
Liver! (they are proteins circulating in the blood)
Glycoproteins; HLA
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

38. what results in symptoms of shock in an acute hemolytic transfusion reaction?
IL 1 and IL 6
Paracortex; viral infection
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

39. What is the clinical use for azathioprine?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
The patient could become cyanotic in the OR!
...

40. What lymph node drains the breast?
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 :(
Axillary
Macrophages - Dendritic cells - B cells
Previous transfusion; pregnant woman whose fetus had paternal antigens

41. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
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
Superior mesenteric
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

42. What are the autoantibodies for myasthenia gravis?
Delayed type hypersensitivity
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
Anti Ach receptor
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 :(

43. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Its a serine protease that activates apoptosis; NK and CD8
Cells that stil have weird parts of their membrane that macrophages usually bite off
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

44. What is the most common example of passive immunity?
IgAs in mothers breast milk!
MHC class molecules bind to KIRS or CD94 to prevent killing
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

45. What are the main cell surface proteins on B cells?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Kill them because they have CD16 on them that recognize the FcG portion
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Cyclosporine - OKT3

46. What are the PALS?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

47. which antibodies can bind complement?
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
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
Axillary
IgM and IgG

48. 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 )
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

49. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
TLR ad nuclear receptors
Hereditary angioedema; PNH
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
Inferior mesenteric

50. where are complements produced?
Superior mesenteric
Liver! (they are proteins circulating in the blood)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Paracortex; viral infection