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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
Subjects
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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 PALS?
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
2. Which cytokines do Th2 release and For what?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Daclizumab; prevent ACUTE rejection of renal transplant
acute phase reactants
3. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
IL 4 - 5 - 10 - 6
acute phase reactants
IgE
4. What is the pathogenesis of acute transplant rejection? When does it occur?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Activate macrophages
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
5. What is the main function of IL 8?
A chemotactic factor for neutrophils
Bind FcG for antibody dependent cellular cytotoxicity
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Activates cytotoxic CD 8 T cells as second signal
6. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Anti alpha subunit 3 of collagen on type IV bm
type four
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
CD56
7. what cell surface proteins are on all APCs?
Antidesmoglein
MHC II - B7
Axillary
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
8. What is the pathology of acute transplant rejection? is it reversible?
Anti U1 RNP (ribonucleoprotein)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
TGF beta and IL 10
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
9. What does granzyme do? who secretes it?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
secondary
Its a serine protease that activates apoptosis; NK and CD8
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
10. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Immunosuppression after kidney transplantation
Influenza; antigenic shift; antigenic drift
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
IL 3; supports growth and differentiation of bone marrow stem cells
11. What are four results of a splenectomy?
Paracortex
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Superficial inguinal
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
12. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgG
False! B cell class switching requires a second signal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
13. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Its a serine protease that activates apoptosis; NK and CD8
Negative nitroblue tetrazolium reduction test
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
14. What are the main Cell surface proteins on T cells?
Increases expression of MHC I and MHC II and also activates NK cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Negative!
15. IgG...
Lymphocytes
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
opsonizes
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
16. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
pale central germinal centers
17. What lymph node drains the anal canal (below the pectinate line)?
cannot cross placenta
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Superficial inguinal
18. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM and IgA
IL 5
19. Which disease is associated with B8?
Graves
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
20. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Previous transfusion; pregnant woman whose fetus had paternal antigens
Glycoproteins; HLA
A recomb cytokine of IL 2; RCC and metastatic melanoma
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
21. what cytokine does basophils secrete?
IL 4
IgM and IgG
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
22. What is the marginal zone of the spleen? what happens there?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Active; passive - fast but short half life (3 weeks!)
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
23. T/F B cells do not require a second signal
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 IgA
False! B cell class switching requires a 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
24. which cells have more complete tolerance - B or T cells?
Edema and necrosis in that region
T
Activate macrophages
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
25. IgM can fix complement but...
C5a
cannot cross placenta
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
26. are Th cells involved in trapping of antigens of endotoxin/LPS?
By transcytosis
No because no peptide fragment!
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
Carbohydrate
27. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
28. What is colostrum?
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 igA found in breast milk
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Thrombocytopenia
29. What is the presentation of scid? treatment?
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 :(
IL 1 and IL 6
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
A j chain
30. What bugs can actually infect the lymph node itself?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
31. IgM can exist as a _______ also
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
pentamer
IgE
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
32. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
33. How fast does it occur?
MS
The patient could become cyanotic in the OR!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Axillary
34. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti TSh receptor
35. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Popliteal
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
active complement pathway
Activate macrophages
36. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Anti Jo -1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
37. What is the treatment of acute transplant rejection?
Basophils! THey want IG E class switch!
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
Cyclosporine - OKT3
C5a
38. What is digoxin immune Fab used for?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antidote for digoxin intoxication
Cytokine IL 10 secreted by Th2
39. What lymph node drains the testes?
2 heavy chains and two light chains
Para aortic
Anti viral and anti tumor
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
40. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Axillary
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
IgG
...
41. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
IgG
42. What is recomb gamma interferon used for?
Chronic granulomatous disease
MHC I - CD16 - CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
delayed!
43. Other than stimulating fever - what else does IL 6 do?
IgM and IgD
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
pathogenesis
Stimulate the liver to release acute phase reactants
44. The idiotype; the Fc portion determines the...
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Glycoproteins; HLA
isotype
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
45. What are the autoantibodies for Mixed connective tissue disease?
secondary
CD56
S. aureus - E. Coli - aspergillus
Anti U1 RNP (ribonucleoprotein)
46. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Negative selection
Not thymus - BM
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
47. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Anti alpha subunit 3 of collagen on type IV bm
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Severe pyogenic infections early in life
48. What are the autoantibodies for wegeners granulomatosis?
MHC class molecules bind to KIRS or CD94 to prevent killing
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
49. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Its a serine protease that activates apoptosis; NK and CD8
Cross link
50. What is the toxicity of muromonab?
Steroid responsive nephrotic syndrome
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Receiving preformed Antibodies
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!