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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. In general What are T cells good for?
Th cells fail to produce interferon gamma; a lot of IgE
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti viral and anti tumor
Local infection/inflammation; infection of the ln itself; metastasis

2. What are the PALS?
Activates cytotoxic CD 8 T cells as second signal
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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

3. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Its a serine protease that activates apoptosis; NK and CD8

4. What are the main cell surface proteins on B cells?
dimer
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
A chemotactic factor for neutrophils
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a

5. What lymph node drains the duodenum - jejunum?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Superior mesenteric
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

6. What is the main function of IL 8?
Anti alpha subunit 3 of collagen on type IV bm
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
A chemotactic factor for neutrophils

7. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
except hyperacute
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

8. What happens in a secondary follicle?
Paracortex
Type IV
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

9. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Anti topoisomerase
Rheumatic arthritis
A recomb cytokine of IL 2; RCC and metastatic melanoma
Activate macrophages

10. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Graves
T cell dysfunction

11. Which is the most abundant antibody in blood?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgG
Th2; Th1
Negative selection

12. How fast does it occur?
Paracortex
The patient could become cyanotic in the OR!
dimer
Anti mitochondrial

13. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
...
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
...

14. Type IV hypersensitivity is i...
B - T - and NK cells
Steroid responsive nephrotic syndrome
not Ab mediated
Th cells fail to produce interferon gamma; a lot of IgE

15. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Not thymus - BM
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

16. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Inferior mesenteric
Its a serine protease that activates apoptosis; NK and CD8
MHC II - B7

17. What are the autoantibodies for myasthenia gravis?
A j chain
TNF alpha and IL1
Anti Ach receptor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

18. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IL 5
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
type four

19. What does CD16 on NK cells do?
Superficial inguinal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgG
Bind FcG for antibody dependent cellular cytotoxicity

20. what cell surface proteins are on all APCs?
MHC II - B7
Anti Jo -1
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti viral and anti tumor

21. The idiotype; the Fc portion determines the...
isotype
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
Viral neutralization of igM and IgG!
Antihistone

22. What is the pathogenesis of a candida skin test?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Glycoproteins; HLA
Delayed type hypersensitivity

23. What is the white pulp of the spleen?
SP infections
Alternative splicing of mRNA
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Celiac

24. What is filgrastim and sargramostim? and What is it used for?
Anti viral and anti tumor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
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

25. Give an example of someone who could get hyperacute transplant rejection.
CRP - C3b - IgM
IgG
Active; passive - fast but short half life (3 weeks!)
Previous transfusion; pregnant woman whose fetus had paternal antigens

26. What are the autoantibodies for Mixed connective tissue disease?
Fab portion
Negative selection
Anti U1 RNP (ribonucleoprotein)
Interferon gamma; Th1

27. How is i Th1 helper cell inhibited?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
IL 4
Cytokine IL 10 secreted by Th2
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

28. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Axillary
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

29. What is the main function of interferons?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgG
Immunoflourescent staining of tissue biopsies

30. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
The patient could become cyanotic in the OR!
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
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

31. 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)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
T
T cell activation; no with CD 4 or CD 8

32. ________ regulate the cell mediated response.
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Pernicious Anemia and Hashimotos
Humoral
Active; passive - fast but short half life (3 weeks!)

33. Name the three opsonins
CRP - C3b - IgM
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Its main effect is a defect in Ab opsonization for killing

34. What are the three types of lymphocytes?
Histamine; post capillary venules - vasodilation
B - T - and NK cells
Macrophages - Dendritic cells - B cells
Negative nitroblue tetrazolium reduction test

35. where do somatic hypermutation and class switching occur?
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
In the germinal center of secondary follicles (In the paler center)
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

36. What is the presentation of common variable immunodef? and What are the labs?
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Antimicrosomal and antithyroglobulin
Th cells fail to produce interferon gamma; a lot of IgE

37. What are the cell surface proteins for Macrophages? which two are for opsonins?
By transcytosis
Activates cytotoxic CD 8 T cells as second signal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

38. What lymph node drains the thigh?
Superficial inguinal
Negative selection
lowest concentration
Secretory component

39. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Activates cytotoxic CD 8 T cells as second signal
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
TLR ad nuclear receptors
T cell activation; no with CD 4 or CD 8

40. What are superantigens? give two examples.
Anti SS- A (anti RO) and Anti SS- B
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

41. What lymph node drains the scrotum?
cannot cross placenta
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Superficial inguinal
Antihistone

42. What does Interferon alpha and beta do? how?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected 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
MS - hay fever - SLE - goodpastures

43. 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
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
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
isotype

44. Describe complement dependent Type II hypersensitivity. Give an example.
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Acts as second signal on B cells to induce class switching to IgE and IgG
IgM and IgD
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

45. What is thrombopoietin used for?
Negative!
dimer
Thrombocytopenia
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)

46. What is epo used for?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anemias (esp due to renal failure)
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

47. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Pernicious Anemia and Hashimotos
except hyperacute

48. Only the _______ contribute to the Fc region
Fc
heavy chains
A - B - C; all the D's
Negative!

49. What are some catalase positive organisms?
lowest concentration
Barrel hoop basement membrane fenestrations
S. aureus - E. Coli - aspergillus
Th cells fail to produce interferon gamma; a lot of IgE

50. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Antimicrosomal and antithyroglobulin
Yes