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Test your basic knowledge |
USMLE Step 1 Immunology
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health-sciences
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usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
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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 else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
Activate macrophages
2. What is muromonab - CD3 (OKT3)
Activates cytotoxic CD 8 T cells as second signal
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
3. Complements are...
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
acute phase reactants
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
4. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
T cell dysfunction
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
5. What is the clinical use for azathioprine?
Paracortex
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
...
6. From where do cytokines come from?
IgG
Axillary
Lymphocytes
Local infection/inflammation; infection of the ln itself; metastasis
7. which B and T cell disorder presents with specifically low IgM?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Yes
Wiskott Aldrich syndrome
TLR ad nuclear receptors
8. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Inferior mesenteric
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
9. Leukocyte adhesion defect presents with...
opsonizes
neutrophilia!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
C5a
10. Which diseases are associated with DR4?
type four
DM type I and RA
C5a
Anti SS- A (anti RO) and Anti SS- B
11. The Fc region is found on the...
Remove encapsulated bacateria
carboxy terminal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Increases expression of MHC I and MHC II and also activates NK cells
12. Which HLA's are included in MHC I? MHC II?
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13. ________ regulate the cell mediated response.
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
By transcytosis
Humoral
14. What are the autoantibodies for Celiac disease?
T cell activation; no with CD 4 or CD 8
isotype
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Active; passive - fast but short half life (3 weeks!)
15. How do you test for type III hypersensitivity?
Daclizumab; prevent ACUTE rejection of renal transplant
Active; passive - fast but short half life (3 weeks!)
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
Immunoflourescent staining of tissue biopsies
16. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
17. are Th cells involved in trapping of antigens of endotoxin/LPS?
Anti smooth muscle
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
No because no peptide fragment!
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
18. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Th2; Th1
T
Antidote for digoxin intoxication
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
19. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
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)
A chemotactic factor for neutrophils
20. What are the two signals required for T cells? what happens after?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
21. How fast does it occur?
IgE
IgG
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
The patient could become cyanotic in the OR!
22. The pathogenesis of contact dermatitis is ________ hypersensitivity
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
type four
23. Describe complement dependent Type II hypersensitivity. Give an example.
Stimulate the liver to release acute phase reactants
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
Its a serine protease that activates apoptosis; NK and CD8
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
24. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Activates Th1 helper cells; Macrophages
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
25. describe the classic complement pathway.
A j chain
Active; passive - fast but short half life (3 weeks!)
Anti mitochondrial
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
26. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antimicrosomal and antithyroglobulin
Anti Jo -1
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
27. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
28. What lymph node drains the thigh?
Superficial inguinal
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Activates cytotoxic CD 8 T cells as second signal
TNF alpha and IL1
29. What is the pathogenesis of acute transplant rejection? When does it occur?
IL 5
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
DM type I
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
30. which antibodies can bind complement?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM and IgG
CRP - C3b - IgM
31. What does IL 4 do?
Wiskott Aldrich syndrome
Anti IF
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
32. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
MHC I - CD16 - CD56
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
...
IgAs in mothers breast milk!
33. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Sinusitis - otitis media - pneumonia
Anti alpha subunit 3 of collagen on type IV bm
Anemias (esp due to renal failure)
34. What is three common causes of severe combined immunodef? What is the result of all three?
Superior mesenteric
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
...
pentamer
35. What is the most common selective Ig deficiency? What is the presentation?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
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
36. which interleukin receptor is required for NK development? activation?
DM type I
TLR ad nuclear receptors
IL 15; IL 12 - interferon Beta and interferon alpha
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
37. where are complements produced?
Liver! (they are proteins circulating in the blood)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Negative nitroblue tetrazolium reduction test
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
38. How is the antigen loaded onto a MHC II?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
TNF alpha and IL1
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
39. which antibodies prevent antigens from binding mucosal surfaces?
IgA
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
40. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
A - B - C; all the D's
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
isotype
41. What is recomb alpha interferon used for?
active complement pathway
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
42. What are C1 - C2 - C3 - C4 important for?
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
Complement activation (active in both)
Viral neutralization of 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
43. Which antibodies can be multimeric?
IL 5
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
pentamer
IgM and IgA
44. What are the autoantibodies for autoimmune hepatitis?
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
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
Negative selection
Anti smooth muscle
45. describe the pathogenesis of delayed type IV hypersensitivity
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Liver! (they are proteins circulating in the blood)
Previous transfusion; pregnant woman whose fetus had paternal antigens
46. What are the main cell surface proteins on B cells?
Hemochromatosis
Its main effect is a defect in Ab opsonization for killing
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
47. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Recom IL 11; thrombocytopenia
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
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
48. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
IgAs in mothers breast milk!
Anti Jo -1
Daclizumab; prevent ACUTE rejection of renal transplant
Rheumatic arthritis
49. Only the _______ contribute to the Fc region
Hemochromatosis
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
heavy chains
A - B - C; all the D's
50. What are the PALS?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Tetanus - Botulinum - HBV - Rabies
pathogenesis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Sorry!:) No result found.
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