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Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
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. which type of immunity is slow but long lasting? as opposed to...
If there is class switching and plasma cell production (that is when memory cells are produced)
Active; passive - fast but short half life (3 weeks!)
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
Popliteal
2. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Anti U1 RNP (ribonucleoprotein)
Anti TSh receptor
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgM and IgG
3. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Cytokine IL 10 secreted by Th2
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
All MHC 1/CD8
4. What are the three types of APCs?
not Ab mediated
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Macrophages - Dendritic cells - B cells
5. What is the pathology of acute transplant rejection? is it reversible?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
carboxy terminal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
6. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
T cell activation; no with CD 4 or CD 8
Steroid responsive nephrotic syndrome
Paracortex
7. 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)?
RNA segment reassortment
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
CRP - C3b - IgM
8. The idiotype; the Fc portion determines the...
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
isotype
9. What are the autoantibodies for other vasculitides?
If there is class switching and plasma cell production (that is when memory cells are produced)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Cyclosporine - OKT3
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
10. What lymph node drains the thigh?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Superficial inguinal
TGF beta and IL 10
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
11. What are the autoantibodies for hashimotos?
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
Remove encapsulated bacateria
Antimicrosomal and antithyroglobulin
Anti topoisomerase
12. How is the antigen loaded onto a MHC II?
Cyclosporine - OKT3
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
type four
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
13. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Glycoproteins; HLA
Immunosuppression after kidney transplantation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
14. What are the cell surface proteins on NK cells?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
MHC I - CD16 - CD56
Antihistone
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
15. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti Jo -1
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
16. The Fc region is found on the...
carboxy terminal
Anti topoisomerase
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)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
17. What is the toxicity of azathioprine?
...
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Histamine; post capillary venules - vasodilation
The igA found in breast milk
18. In general What are T cells good for?
Yes
Anti viral and anti tumor
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
MHC I; from RER with help of the B2 microglobulin
19. What are the autoantibodies for Mixed connective tissue disease?
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
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
Anti U1 RNP (ribonucleoprotein)
TGF beta and IL 10
20. Which diseases are associated with DR4?
IgE; by activating eosinophils
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
secondary
DM type I and RA
21. What does IL 4 do?
IgAs in mothers breast milk!
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 4 - 5 - 10 - 6
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
22. What are howell jolly bodies?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Carbohydrate
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
23. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Thrombocytopenia
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
24. What are the autoantibodies for pemphigus bulgaris?
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!
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antidesmoglein
25. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TNF alpha and IL1
IgM and IgA
26. What does interferon gamma do? What two type of cells does it attack mostly?
IgAs in mothers breast milk!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 3; supports growth and differentiation of bone marrow stem cells
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
27. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Edema and necrosis in that region
IgE
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
28. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
IgM and IgD
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
except hyperacute
29. How is the thymus organized? what happens in each section?
TLR ad nuclear receptors
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
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
Axillary
30. What is a factor that is a predictor for a bad transplantation?
MHC I - CD16 - CD56
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
31. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
TLR ad nuclear receptors
Lymphocytes
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
32. Which diseases are associated with DR2?
Celiac
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MS - hay fever - SLE - goodpastures
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
33. which antibody activate mast cells - basophils - and eosinophils?
Bind FcG for antibody dependent cellular cytotoxicity
IgE
type four
Axillary
34. What are the mediators that mast cells release?
Humoral
carboxy terminal
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cross link
35. What is the main function of IL 8?
isotype
Antidote for digoxin intoxication
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
A chemotactic factor for neutrophils
36. other than C3a - what other complement acts as an anaphyloxin?
Rheumatic arthritis
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IgM and IgG
C5a
37. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Paracortex; viral infection
Graves
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
38. What are the autoantibodies for primary biliary cirrhosis?
MHC I - CD16 - CD56
IgM and IgA
All MHC 1/CD8
Anti mitochondrial
39. What are the main Cell surface proteins on T cells?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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 :(
40. what will NK cells do to cells covered in IgG Ab? why?
Superficial inguinal
pentamer
Alternative splicing of mRNA
Kill them because they have CD16 on them that recognize the FcG portion
41. What is chronic mucocutaneous candidiasis d/t?
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
Influenza; antigenic shift; antigenic drift
T cell dysfunction
TGF beta and IL 10
42. 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?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Influenza; antigenic shift; antigenic drift
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
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
43. What are the autoantibodies for pernicious anemia?
RNA segment reassortment
Anti IF
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
Kill them because they have CD16 on them that recognize the FcG portion
44. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Yes
Cytokine IL 10 secreted by Th2
IgE
Paracortex
45. What is the defect in hyper IgM syndrome? What are the lab results?
IgM and IgD
T
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
46. Type IV hypersensitivity is i...
not Ab mediated
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
heavy chains
Pernicious Anemia and Hashimotos
47. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
except hyperacute
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
48. What does IL 10 do? who is secreted by?
MHC II - B7
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
Chronic granulomatous disease
49. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Humoral
Internal iliac
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
50. Name two endogenous pyrogens
IgE; by activating eosinophils
IL 1 and IL 6
Viral neutralization of igM and IgG!
Fab portion