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 pathology in hyperacute transplant rejection?
opsonizes
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
pathogenesis
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

2. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Basophils! THey want IG E class switch!
lowest concentration
IgG

3. which antibody is involved in the primary response or immediate response to an antigen?
Internal iliac
Kill them because they have CD16 on them that recognize the FcG portion
IgM
active complement pathway

4. What is passive immunity?
Kill them because they have CD16 on them that recognize the FcG portion
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Receiving preformed Antibodies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

5. T/F B cells do not require a second signal
Anti IF
False! B cell class switching requires a second signal
Carbohydrate
CRP - C3b - IgM

6. What does interferon gamma do? What two type of cells does it attack mostly?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Daclizumab; prevent ACUTE rejection of renal transplant
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Liver! (they are proteins circulating in the blood)

7. The idiotype; the Fc portion determines the...
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
False! B cell class switching requires a second signal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
isotype

8. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
pentamer
Anti glutamate carboxylase and anti insulin
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

9. What lymph node drains the scrotum?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Hemochromatosis
Superficial inguinal
T cell dysfunction

10. What are some sinopulmonary infections?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Glycoproteins; HLA
Sinusitis - otitis media - pneumonia

11. Which disease is associated withB B27?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

12. Name two endogenous pyrogens
IL 1 and IL 6
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immunosuppression after kidney transplantation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

13. How does complement link innate and adaptive?
IgE
CRP - C3b - IgM
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM

14. Which is the main antibody that provides passive immunity to infants?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgG
opsonizes
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

15. What is the toxicity of muromonab?
SP infections
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
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

16. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
Paracortex; viral infection
Negative selection
All MHC 1/CD8

17. are Th cells involved in trapping of antigens of endotoxin/LPS?
IgE
No because no peptide fragment!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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

18. in which immunodef order do you see a lot of pus? no pus?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
All MHC 1/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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

19. What is the most common selective Ig deficiency? What is the presentation?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

20. what ensure that a memory response is generated?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC I - CD16 - CD56
If there is class switching and plasma cell production (that is when memory cells are produced)
Negative!

21. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Superior mesenteric
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
lowest concentration

22. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Fab portion
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

23. Give an example of someone who could get hyperacute transplant rejection.
neutrophilia!
Previous transfusion; pregnant woman whose fetus had paternal antigens
Delayed type hypersensitivity
not Ab mediated

24. What is the main function of TNF alpha? How does it do this?
Sinusitis - otitis media - pneumonia
IL 3; supports growth and differentiation of bone marrow stem cells
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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. is IgM an opsonizer?
Activates cytotoxic CD 8 T cells as second signal
Negative!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

26. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
MS - hay fever - SLE - goodpastures
NK cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

27. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
MHC I - CD16 - CD56
carboxy terminal
TNF alpha and IL1

28. 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
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 :(
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgM and IgA

29. Complements are...
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
acute phase reactants
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

30. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Th cells fail to produce interferon gamma; a lot of IgE
IgM and IgD

31. How do you test for type III hypersensitivity?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Immunoflourescent staining of tissue biopsies
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
delayed!

32. What is the main cytokine that activates eosinophils?
IL 5
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

33. What does granzyme do? who secretes it?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anemias (esp due to renal failure)
Its a serine protease that activates apoptosis; NK and CD8

34. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
pale central germinal centers
Fab portion
carboxy terminal

35. What are the main symptoms of B cell immunodeficiencies?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
SP infections
isotype

36. What does Interferon alpha and beta do? how?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IgG

37. What is the receptor for EBV? On what cells is that located?
Activate macrophages
Cyclosporine - OKT3
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
CD21 on B cells (although there is T cell lymphocytosis in EBV)

38. What is chronic mucocutaneous candidiasis d/t?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
T cell dysfunction
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

39. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
IgA
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
Its main effect is a defect in Ab opsonization for killing

40. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Axillary
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Popliteal
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

41. 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
active complement pathway
No because no peptide fragment!
When you select for which MHC it will have; take out the lymphs that self react

42. What lymph node drains the breast?
Carbohydrate
Inferior mesenteric
cannot cross placenta
Axillary

43. What is the main function of IL 8?
IgG
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A chemotactic factor for neutrophils
Daclizumab; prevent ACUTE rejection of renal transplant

44. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
mesenchymal
except hyperacute
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

45. The MALT/GALT are not...
pathogenesis
encapsulated
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

46. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Daclizumab; prevent ACUTE rejection of renal transplant
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

47. What are the autoantibodies for graves?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti TSh receptor
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

48. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IgM and IgD
Interferon gamma; Th1
Antibody mediated cytotoxicity; either complement dependent or complement independent

49. What links the adaptive and innate immunity?
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
DM type I
Complement activation (active in both)
Macrophages - Dendritic cells - B cells

50. What lymph node drains the testes?
Para aortic
DM type I and RA
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T cell precursor