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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.
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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 the autoantibodies for myasthenia gravis?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti Jo -1
Anti Ach receptor
Anti SS- A (anti RO) and Anti SS- B

2. which of the transplant rejections is antibody mediated? why does it occur?
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
...
RNA segment reassortment

3. What are the two signals required for Th1 cells? what happens after then activated?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Hemochromatosis
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

4. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
IL 1 and IL 6
Alternative splicing of mRNA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
All MHC 1/CD8

5. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
A - B - C; all the D's
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
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

6. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
Hereditary angioedema; PNH

7. What is three common causes of severe combined immunodef? What is the result of all three?
MHC I; from RER with help of the B2 microglobulin
Popliteal
IgE; by activating eosinophils
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

8. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Anti smooth muscle
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
In the germinal center of secondary follicles (In the paler center)

9. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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)
except hyperacute
Acts as second signal on B cells to induce class switching to IgE and IgG

10. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti Ach receptor
isotype
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

11. where do NK cells develop?
Not thymus - BM
Activate macrophages
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

12. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Wiskott Aldrich syndrome
Acts as second signal on B cells to induce class switching to IgE and IgG

13. when can graft versus host disease? What is the result?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Superficial inguinal
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
Active; passive - fast but short half life (3 weeks!)

14. What are the autoantibodies for Mixed connective tissue disease?
Graves
Paracortex
Anti U1 RNP (ribonucleoprotein)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

15. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Antibody mediated cytotoxicity; either complement dependent or complement independent
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Immunosuppression after kidney transplantation

16. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
A recomb cytokine of IL 2; RCC and metastatic melanoma

17. Which diseases are associated with DR5?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Pernicious Anemia and Hashimotos
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

18. What lymph node drains the scrotum?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
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
Superficial inguinal

19. How does igA cross the epithelium?
By transcytosis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
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

20. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anti TSh receptor
Axillary
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

21. ________ regulate the cell mediated response.
Antibody mediated cytotoxicity; either complement dependent or complement independent
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Humoral

22. What is the receptor for EBV? On what cells is that located?
T cell precursor
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

23. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Alternative splicing of mRNA
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

24. From where do cytokines come from?
acute phase reactants
Lymphocytes
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

25. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Cyclosporine - OKT3
T cell dysfunction
Not thymus - BM

26. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
pathogenesis
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

27. What are the two signals required for B cell class switching? Which is the second signal?
Anti SS- A (anti RO) and Anti SS- B
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
neutrophilia!
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

28. Which helper T cells' development is induced by IL 4? IL 12?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Th2; Th1
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
IgM and IgD

29. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
pathogenesis
Anti Ach receptor
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

30. To what portion of the Antibody do the complements bind?
IgG
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
T cell activation; no with CD 4 or CD 8
Fc

31. How do you test for type III hypersensitivity?
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Immunoflourescent staining of tissue biopsies
IL 15; IL 12 - interferon Beta and interferon alpha

32. What is recomb beta interferon used for?
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
2 heavy chains and two light chains
MS
dimer

33. What are the T cell functions?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Edema and necrosis in that region
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

34. Which disease is associated with HLA A3?
Anti Jo -1
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Hemochromatosis
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

35. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
pale central germinal centers
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
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
Carbohydrate

36. What lymph node drains the sigmoid colon?
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
Inferior mesenteric
Anti topoisomerase
IL 1 and IL 6

37. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Barrel hoop basement membrane fenestrations
Internal iliac

38. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Antihistone
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
delayed!
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

39. What is the general structure of an Ab?
Anti mitochondrial
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
2 heavy chains and two light chains

40. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Anti Jo -1
Carbohydrate
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

41. 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
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

42. What is the pathogenesis of a candida skin test?
Rheumatic arthritis
If there is class switching and plasma cell production (that is when memory cells are produced)
Delayed type hypersensitivity
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

43. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
cannot cross placenta
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
delayed!

44. What is the mechanism for sirolimus? what else it known as?
Interferon gamma and IL 2
False! B cell class switching requires a second signal
MHC I - CD16 - CD56
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

45. Only the _______ contribute to the Fc region
Anti mitochondrial
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
heavy chains
Histamine; post capillary venules - vasodilation

46. What is recomb gamma interferon used for?
A - B - C; all the D's
Chronic granulomatous disease
Basophils! THey want IG E class switch!
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

47. Which diseases are associated with DR4?
DM type I and RA
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
SP infections
IL 4

48. What does interferon gamma do to be antiviral?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
Increases expression of MHC I and MHC II and also activates NK cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

49. Describe the Mannose Lectin pathway
IgM and IgD
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Thrombocytopenia
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

50. Complements are...
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
mesenchymal
acute phase reactants
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L