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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
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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 a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Graves
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgA
2. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Its main effect is a defect in Ab opsonization for killing
Glycoproteins; HLA
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
3. Other than stimulating fever - what else does IL 6 do?
IgG
Histamine; post capillary venules - vasodilation
Stimulate the liver to release acute phase reactants
Paracortex; viral infection
4. What are the autoantibodies for pernicious anemia?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
T cell precursor
Rheumatic arthritis
Anti IF
5. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
6. What is immune complex disease? give an example.
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti SS- A (anti RO) and Anti SS- B
Glycoproteins; HLA
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
7. What is the pathology in hyperacute transplant rejection?
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
delayed!
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Viral neutralization of igM and IgG!
8. what ensure that a memory response is generated?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Interferon gamma and IL 2
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
If there is class switching and plasma cell production (that is when memory cells are produced)
9. What is the late phase reaction of anaphylaxis allergy? what mediates it?
DM type I
Edema and necrosis in that region
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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)
10. Which disease is associated with DR3?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IL 15; IL 12 - interferon Beta and interferon alpha
Anti Jo -1
DM type I
11. What is the pathology of acute transplant rejection? is it reversible?
Lymphocytes
MHC II - B7
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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. __________ are a part of the innate system.
MS - hay fever - SLE - goodpastures
Sinusitis - otitis media - pneumonia
NK cells
IL 4
13. What are the symptoms of serum sickness?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
MHC I; from RER with help of the B2 microglobulin
14. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Negative!
15. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Remove encapsulated bacateria
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti U1 RNP (ribonucleoprotein)
16. What does CD16 on NK cells do?
In the germinal center of secondary follicles (In the paler center)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Bind FcG for antibody dependent cellular cytotoxicity
17. What are the main symptoms of B cell immunodeficiencies?
Anti Ach receptor
Anti TSh receptor
SP infections
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
18. What are the two signals to kill for NK cells?
Complement activation (active in both)
IgM and IgD
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
19. What is the toxicity of muromonab?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti glutamate carboxylase and anti insulin
All MHC 1/CD8
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
20. what cytokine does basophils secrete?
IL 4
Superficial inguinal
Type IV
Remove encapsulated bacateria
21. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
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
The igA found in breast milk
active complement pathway
22. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Interferon gamma; Th1
Histamine; post capillary venules - vasodilation
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
acute phase reactants
23. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
B - T - and NK cells
pathogenesis
Histamine; post capillary venules - vasodilation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
24. Which diseases are associated with DR2?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Th cells fail to produce interferon gamma; a lot of IgE
MS - hay fever - SLE - goodpastures
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
25. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
T cell dysfunction
type four
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
26. Type Iv hypersensitivity is...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
delayed!
Previous transfusion; pregnant woman whose fetus had paternal antigens
Sinusitis - otitis media - pneumonia
27. What are the autoantibodies for Mixed connective tissue disease?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti U1 RNP (ribonucleoprotein)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
acute phase reactants
28. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Recom IL 11; thrombocytopenia
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
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
29. What does IL 4 do?
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
Anti Jo -1
Wiskott Aldrich syndrome
Acts as second signal on B cells to induce class switching to IgE and IgG
30. T/F B cells do not require a second signal
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
False! B cell class switching requires a second signal
C5a
Histamine; post capillary venules - vasodilation
31. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IgE; by activating eosinophils
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Complement activation (active in both)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
32. What is colostrum?
IgM and IgA
Activates Th1 helper cells; Macrophages
The igA found in breast milk
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
33. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
B - T - and NK cells
Carbohydrate
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
34. What is the main function of IL 8?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti topoisomerase
A chemotactic factor for neutrophils
35. can igG cross the placenta?
Bind FcG for antibody dependent cellular cytotoxicity
IgG
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Yes
36. What are the three types of APCs?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
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
Macrophages - Dendritic cells - B cells
37. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
38. The Fc region is found on the...
Severe pyogenic infections early in life
carboxy terminal
Fc
TLR ad nuclear receptors
39. For which toxins are preformed antibodies (passive) given?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Tetanus - Botulinum - HBV - Rabies
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
Anemias (esp due to renal failure)
40. What is chronic mucocutaneous candidiasis d/t?
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
T cell dysfunction
41. 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!
MHC II - B7
T cell dysfunction
encapsulated
42. What are C1 - C2 - C3 - C4 important for?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgG
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Viral neutralization of igM and IgG!
43. ________ regulate the cell mediated response.
Humoral
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti IF
Anti SS- A (anti RO) and Anti SS- B
44. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
A - B - C; all the D's
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
45. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Active; passive - fast but short half life (3 weeks!)
All MHC 1/CD8
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
46. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Active; passive - fast but short half life (3 weeks!)
47. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Th cells fail to produce interferon gamma; a lot of IgE
Activate macrophages
Activates cytotoxic CD 8 T cells as second signal
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
48. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Basophils! THey want IG E class switch!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
49. The alternative pathway is the only constutively...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti topoisomerase
active complement pathway
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 :(
50. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
A - B - C; all the D's
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp