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Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
Study First
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 are the main symptoms of B cell immunodeficiencies?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Fc
SP infections
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
2. Which MHC presents intracellular peptides? how so?
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
MHC I; from RER with help of the B2 microglobulin
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
3. other than eat and bite RBCs what else do Macrophages of spleen do>
Paracortex; viral infection
Inferior mesenteric
Remove encapsulated bacateria
Antidote for digoxin intoxication
4. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
CD56
Anemias (esp due to renal failure)
Anti viral and anti tumor
5. What is the common variable immunodeficiency ? How is it different from Brutons?
mesenchymal
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
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
6. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Wiskott Aldrich syndrome
TGF beta and IL 10
pale central germinal centers
7. which antibodies can bind complement?
IgM and IgG
Its a serine protease that activates apoptosis; NK and CD8
Delayed type hypersensitivity
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
8. Which disease is associated with HLA A3?
secondary
IgG
2 heavy chains and two light chains
Hemochromatosis
9. which antibody is involved in the primary response or immediate response to an antigen?
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
pathogenesis
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgM
10. which antibodies prevent antigens from binding mucosal surfaces?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
IgA
11. The idiotype; the Fc portion determines the...
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 :(
All MHC 1/CD8
isotype
Immunoflourescent staining of tissue biopsies
12. which cytokine inhibits TH2 cells? secreted by who?
Viral neutralization of igM and IgG!
Interferon gamma; Th1
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
TLR ad nuclear receptors
13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Superficial inguinal
If there is class switching and plasma cell production (that is when memory cells are produced)
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
14. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Axillary
Negative selection
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
15. What are the T cell functions?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
lowest concentration
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
16. What lymph node drains the rectum (above the pectinate line)?
Anti TSh receptor
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
Internal iliac
acute phase reactants
17. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
IL 1 and IL 6
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
C5a
18. What cytokines are released by Th1 cells?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Interferon gamma and IL 2
Th2; Th1
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
19. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Complement activation (active in both)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Wiskott Aldrich syndrome
A chemotactic factor for neutrophils
20. Name the three opsonins
IL 4
CRP - C3b - IgM
carboxy terminal
MS
21. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti mitochondrial
Anemias (esp due to renal failure)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
22. What is an example of a parasite showing antigenic variation?
Th2; Th1
Internal iliac
TNF alpha and IL1
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
23. What is the main function of IL 12? other than macrophages who else can release IL 12?
Celiac
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
Tetanus - Botulinum - HBV - Rabies
24. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IL 1 and IL 6
Anemias (esp due to renal failure)
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
25. hat is the presentation of Jobs syndrome or Hyper IgE?
IgM and IgG
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
26. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Its a serine protease that activates apoptosis; NK and CD8
Superficial inguinal
pentamer
27. The MALT/GALT are not...
Celiac
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
isotype
encapsulated
28. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
29. what cell surface proteins are on all APCs?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Interferon gamma; Th1
MHC II - B7
Liver! (they are proteins circulating in the blood)
30. What is the defect in hyper IgM syndrome? What are the lab results?
Influenza; antigenic shift; antigenic drift
A recomb cytokine of IL 2; RCC and metastatic melanoma
Activate macrophages
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
31. Which is the main antibody that provides passive immunity to infants?
IgG
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti IF
IgAs in mothers breast milk!
32. __________ are a part of the innate system.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
NK cells
Not thymus - BM
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
33. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Stimulate the liver to release acute phase reactants
T cell precursor
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
34. How is i Th1 helper cell inhibited?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Cytokine IL 10 secreted by Th2
35. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
MHC II - B7
Complement activation (active in both)
Sinusitis - otitis media - pneumonia
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
36. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Stimulate the liver to release acute phase reactants
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
A j chain
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
37. what prevents NK cells from killing normal cells if their default is to kill?
Anti TSh receptor
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
MHC class molecules bind to KIRS or CD94 to prevent killing
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
38. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti Jo -1
Immunoflourescent staining of tissue biopsies
39. What do mature naive B lymphocytes express?
Antimicrosomal and antithyroglobulin
IgM and IgD
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
Its a serine protease that activates apoptosis; NK and CD8
40. are Th cells involved in trapping of antigens of endotoxin/LPS?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
No because no peptide fragment!
TGF beta and IL 10
Anti glutamate carboxylase and anti insulin
41. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
CRP - C3b - IgM
42. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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!
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti TSh receptor
43. where are complements produced?
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
Bind FcG for antibody dependent cellular cytotoxicity
Liver! (they are proteins circulating in the blood)
TGF beta and IL 10
44. What is oprelevkin? and What is it used for?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Recom IL 11; thrombocytopenia
Hemochromatosis
Inferior mesenteric
45. Name 5 ways Antibody diversity is generated?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
46. which antibody activate mast cells - basophils - and eosinophils?
C5a
IgE
Its main effect is a defect in Ab opsonization for killing
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
47. How fast does it occur?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Viral neutralization of igM and IgG!
The patient could become cyanotic in the OR!
48. IgM can exist as a _______ also
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
pentamer
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
CD56
49. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Hemochromatosis
RNA segment reassortment
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
Daclizumab; prevent ACUTE rejection of renal transplant
50. IgG...
T cell dysfunction
Type IV
opsonizes
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor