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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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1. What type of fenestrations are found in the red pulp of the spleen?
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
Increases expression of MHC I and MHC II and also activates NK cells
Barrel hoop basement membrane fenestrations
B - T - and NK cells

2. What are the autoantibodies for goodpastures syndrome?
Its main effect is a defect in Ab opsonization for killing
Anti alpha subunit 3 of collagen on type IV bm
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
RNA segment reassortment

3. What are four results of a splenectomy?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
S. aureus - E. Coli - aspergillus
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

4. The alternative pathway is the only constutively...
Cells that stil have weird parts of their membrane that macrophages usually bite off
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
active complement pathway
Immunoflourescent staining of tissue biopsies

5. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Kill them because they have CD16 on them that recognize the FcG portion
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
MS - hay fever - SLE - goodpastures

6. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Local infection/inflammation; infection of the ln itself; metastasis
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

7. what will NK cells do to cells covered in IgG Ab? why?
IgM and IgG
Kill them because they have CD16 on them that recognize the FcG portion
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
type four

8. What are superantigens? give two examples.
Sinusitis - otitis media - pneumonia
acute phase reactants
TNF alpha and IL1
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

9. IgM can fix complement but...
cannot cross placenta
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

10. What does IL 4 do?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 4 - 5 - 10 - 6
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti glutamate carboxylase and anti insulin

11. Which antibody mediates immunity to worms? how?
T cell dysfunction
Superficial inguinal
IgE; by activating eosinophils
Activates cytotoxic CD 8 T cells as second signal

12. What lymph node drains the testes?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Para aortic

13. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Cytokine IL 10 secreted by Th2
...
CD56

14. which B and T cell disorder presents with specifically low IgM?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Wiskott Aldrich syndrome
Chronic granulomatous disease

15. What cytokines to Th2 secrete?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IL 4 - 5 - 10 - 6
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
MS - hay fever - SLE - goodpastures

16. describe the pathogenesis of delayed type IV hypersensitivity
Anti IF
cannot cross placenta
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Negative nitroblue tetrazolium reduction test

17. 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?
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
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

18. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Axillary
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

19. What is filgrastim and sargramostim? and What is it used for?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Paracortex
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

20. What does interferon gamma do to be antiviral?
Thrombocytopenia
Cyclosporine - OKT3
Increases expression of MHC I and MHC II and also activates NK cells
Internal iliac

21. Complements are...
Chronic granulomatous disease
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
acute phase reactants
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

22. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Thrombocytopenia
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

23. What lymph node drains the duodenum - jejunum?
Its a serine protease that activates apoptosis; NK and CD8
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Superior mesenteric

24. What do multimeric antibodies require for assembly?
Severe pyogenic infections early in life
A j chain
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
acute phase reactants

25. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

26. what prevents NK cells from killing normal cells if their default is to kill?
Cells that stil have weird parts of their membrane that macrophages usually bite off
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti U1 RNP (ribonucleoprotein)
pathogenesis

27. What are the PALS?
Anti Jo -1
Superior mesenteric
Steroid responsive nephrotic syndrome
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

28. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
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

29. How is the thymus organized? what happens in each section?
Cytokine IL 10 secreted by Th2
Macrophages - Dendritic cells - B 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
IgAs in mothers breast milk!

30. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Macrophages - Dendritic cells - B cells
DM type I and RA
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

31. Which disease is associated with DR3?
DM type I
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Not thymus - BM
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

32. which antibodies can bind complement?
NK cells
Axillary
IgM and IgG
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

33. What do mature naive B lymphocytes express?
IgM and IgD
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti U1 RNP (ribonucleoprotein)
Influenza; antigenic shift; antigenic drift

34. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
TGF beta and IL 10
IL 15; IL 12 - interferon Beta and interferon alpha
Rheumatic arthritis

35. What lymph node drains the sigmoid colon?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Inferior mesenteric
Lymphocytes
Para aortic

36. The idiotype; the Fc portion determines the...
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
isotype
Activate macrophages
Anti alpha subunit 3 of collagen on type IV bm

37. What can cause a lymph node enlargement?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Local infection/inflammation; infection of the ln itself; metastasis
IgE; by activating eosinophils
Its main effect is a defect in Ab opsonization for killing

38. when can graft versus host disease? What is the result?
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
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
Anti SS- A (anti RO) and Anti SS- B
B - T - and NK cells

39. What is the main function of TNF alpha? How does it do this?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
IgM and IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

40. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
lowest concentration
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

41. To what portion of the Antibody do the complements bind?
Antihistone
Local infection/inflammation; infection of the ln itself; metastasis
Fc
MHC I - CD16 - CD56

42. What is colostrum?
Th cells fail to produce interferon gamma; a lot of IgE
A - B - C; all the D's
The igA found in breast milk
Paracortex; viral infection

43. IgG...
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
opsonizes

44. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

45. 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)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Basophils! THey want IG E class switch!
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

46. What are the autoantibodies for drug induced lupus?
neutrophilia!
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Antihistone

47. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Immunoflourescent staining of tissue biopsies
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
Its a serine protease that activates apoptosis; NK and CD8

48. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
except hyperacute
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

49. What is the clinical use for azathioprine?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
...
mesenchymal
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

50. where are complements produced?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Alternative splicing of mRNA
MHC class molecules bind to KIRS or CD94 to prevent killing
Liver! (they are proteins circulating in the blood)