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. What is the pathogenesis of a candida skin test?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
DM type I and RA
Delayed type hypersensitivity

2. What bugs can actually infect the lymph node itself?
Celiac
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Anti IF
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

3. What are the two signals to kill for NK cells?
T cell activation; no with CD 4 or CD 8
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti topoisomerase

4. What is the white pulp of the spleen?
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
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

5. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

6. What is epo used for?
Anemias (esp due to renal failure)
All MHC 1/CD8
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

7. What cytokines to Th2 secrete?
Anti TSh receptor
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
SP infections
IL 4 - 5 - 10 - 6

8. What lymph node drains the breast?
Glycoproteins; HLA
Axillary
Cytokine IL 10 secreted by Th2
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

9. What are the autoantibodies for drug induced lupus?
Antihistone
MHC II - B7
IgM and IgG
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

10. What is hereditary angioedema? What are the C3 levels?
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
...
Its main effect is a defect in Ab opsonization for killing
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

11. What happens in a deficiency of C3?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
delayed!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

12. which cytokine inhibits TH2 cells? secreted by who?
When you select for which MHC it will have; take out the lymphs that self react
Interferon gamma; Th1
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

13. What are the function of B cells?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

14. Which are the only two antiinflammatory cytokines?
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
TGF beta and IL 10
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

15. What lymph node drains the lateral side of the dorsum of the foot?
Acts as second signal on B cells to induce class switching to IgE and IgG
Popliteal
IgM and IgG
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

16. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Influenza; antigenic shift; antigenic drift

17. Which disease is associated with DR7?
isotype
Steroid responsive nephrotic syndrome
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

18. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Negative selection
2 heavy chains and two light chains
Superficial inguinal

19. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
Receiving preformed Antibodies

20. What are some catalase positive organisms?
Anti alpha subunit 3 of collagen on type IV bm
Edema and necrosis in that region
S. aureus - E. Coli - aspergillus
T cell activation; no with CD 4 or CD 8

21. What is a factor that is a predictor for a bad transplantation?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Not thymus - BM
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

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

23. which antibodies can bind complement?
IgM and IgG
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
MHC I - CD16 - CD56

24. What does interferon gamma do? What two type of cells does it attack mostly?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Daclizumab; prevent ACUTE rejection of renal transplant
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

25. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
except hyperacute
A recomb cytokine of IL 2; RCC and metastatic melanoma

26. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Th2; Th1
not Ab mediated
TNF alpha and IL1
Histamine; post capillary venules - vasodilation

27. What is the main cytokine released by T cells? What does it do
Axillary
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 3; supports growth and differentiation of bone marrow stem cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

28. Which antibodies can be multimeric?
IgM and IgA
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
Hemochromatosis
Pernicious Anemia and Hashimotos

29. Other than stimulating fever - what else does IL 6 do?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
Stimulate the liver to release acute phase reactants
IgG

30. What is recomb gamma interferon used for?
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
Chronic granulomatous disease
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgE; by activating eosinophils

31. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgG
T cell dysfunction
Remove encapsulated bacateria

32. which antibodies prevent antigens from binding mucosal surfaces?
IgA
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Remove encapsulated bacateria
2 heavy chains and two light chains

33. other than eat and bite RBCs what else do Macrophages of spleen do>
Its a serine protease that activates apoptosis; NK and CD8
Stimulate the liver to release acute phase reactants
TLR ad nuclear receptors
Remove encapsulated bacateria

34. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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)
Hereditary angioedema; PNH
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
Kill them because they have CD16 on them that recognize the FcG portion

35. What are the autoantibodies for other vasculitides?
Local infection/inflammation; infection of the ln itself; metastasis
not Ab mediated
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

36. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Paracortex
heavy chains
Activate macrophages
IgE; by activating eosinophils

37. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Rheumatic arthritis

38. What lymph node drains the sigmoid colon?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Inferior mesenteric
Activate macrophages
Negative nitroblue tetrazolium reduction test

39. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Fab portion
Anti TSh receptor
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
MS - hay fever - SLE - goodpastures

40. The lymphocytes are ________ origin
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
mesenchymal
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
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

41. what bacteria are a splenectomy patient most susceptible to? why?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
When you select for which MHC it will have; take out the lymphs that self react
Paracortex

42. can igG cross the placenta?
Yes
Severe pyogenic infections early in life
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Paracortex

43. What do multimeric antibodies require for assembly?
Its main effect is a defect in Ab opsonization for killing
IgG
A j chain
IgE; by activating eosinophils

44. What kinds of receptors activate innate immunity?
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
TLR ad nuclear receptors

45. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
MHC class molecules bind to KIRS or CD94 to prevent killing

46. What links the adaptive and innate immunity?
Complement activation (active in both)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IL 4
Active; passive - fast but short half life (3 weeks!)

47. What is the general structure of an Ab?
2 heavy chains and two light chains
Complement activation (active in both)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Internal iliac

48. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Interferon gamma; Th1
Superficial inguinal
False! B cell class switching requires a second signal

49. 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?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Local infection/inflammation; infection of the ln itself; metastasis

50. Complements are...
Influenza; antigenic shift; antigenic drift
Superficial inguinal
acute phase reactants
Sinusitis - otitis media - pneumonia