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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 lymph node drains the testes?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Para aortic
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
2. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Paracortex
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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 :(
3. What is the main cytokine that activates eosinophils?
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
IL 5
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
4. What does granzyme do? who secretes it?
MHC class molecules bind to KIRS or CD94 to prevent killing
Delayed type hypersensitivity
Its a serine protease that activates apoptosis; NK and CD8
TGF beta and IL 10
5. What are target cells?
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
Delayed type hypersensitivity
Cells that stil have weird parts of their membrane that macrophages usually bite off
dimer
6. Describe the complement independent Type II hypersenstivity reaction. Give an example.
A - B - C; all the D's
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
7. What is the main function of interferons?
Humoral
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
T cell activation; no with CD 4 or CD 8
Local infection/inflammation; infection of the ln itself; metastasis
8. What lymph node drains the breast?
Axillary
Superficial inguinal
Th cells fail to produce interferon gamma; a lot of IgE
Antidote for digoxin intoxication
9. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
isotype
10. What are the autoantibodies for type I diabetes mellitus?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
Anti glutamate carboxylase and anti insulin
T
11. What lymph node drains the stomach?
Type IV
Celiac
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Wiskott Aldrich syndrome
12. What are superantigens? give two examples.
Hemochromatosis
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T
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
13. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
heavy chains
CD56
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 :(
14. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
15. what prevents NK cells from killing normal cells if their default is to kill?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MHC class molecules bind to KIRS or CD94 to prevent killing
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
16. What are the autoantibodies for wegeners granulomatosis?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
B - T - and NK cells
MHC I - CD16 - CD56
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
17. What is the pathogenesis of acute transplant rejection? When does it occur?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
18. IgE has the ___________ in the serum
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
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
lowest concentration
19. What are howell jolly bodies?
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
IL 1 and IL 6
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgM and IgG
20. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Activates Th1 helper cells; Macrophages
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
21. which antibody is involved in the primary response or immediate response to an antigen?
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
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
22. what cytokine does basophils secrete?
Its a serine protease that activates apoptosis; NK and CD8
Rheumatic arthritis
IL 4
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
23. What is the pathogenesis of a hypersensitivity reaction?
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 :(
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
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
24. which type of immunity is slow but long lasting? as opposed to...
Carbohydrate
Humoral
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Active; passive - fast but short half life (3 weeks!)
25. where do somatic hypermutation and class switching occur?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Local infection/inflammation; infection of the ln itself; metastasis
In the germinal center of secondary follicles (In the paler center)
26. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Sinusitis - otitis media - pneumonia
Steroid responsive nephrotic syndrome
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
27. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgA
Anti SS- A (anti RO) and Anti SS- B
28. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Hereditary angioedema; PNH
29. Which is the main antibody that provides passive immunity to infants?
Chronic granulomatous disease
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
secondary
30. Which diseases are associated with DR5?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
IL 15; IL 12 - interferon Beta and interferon alpha
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Pernicious Anemia and Hashimotos
31. What cytokines are released by Th1 cells?
Chronic granulomatous disease
Interferon gamma and IL 2
IgM and IgA
IgG
32. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Receiving preformed Antibodies
Increases expression of MHC I and MHC II and also activates NK cells
33. What happens in a deficiency of C3?
dimer
IgM and IgA
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
MHC I; from RER with help of the B2 microglobulin
34. How do you test for chronic granulomatous disease?
Steroid responsive nephrotic syndrome
Negative nitroblue tetrazolium reduction test
carboxy terminal
Inferior mesenteric
35. A lymph node is a ________ lymphoid organ.
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Lymphocytes
MHC I; from RER with help of the B2 microglobulin
secondary
36. What does interferon gamma do? What two type of cells does it attack mostly?
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Viral neutralization of igM and IgG!
37. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgE
38. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
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
39. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
40. What is passive immunity?
IgE
Receiving preformed Antibodies
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
41. What are the autoantibodies for sjorgens syndrome?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
opsonizes
Immunoflourescent staining of tissue biopsies
Anti SS- A (anti RO) and Anti SS- B
42. What do mature naive B lymphocytes express?
Influenza; antigenic shift; antigenic drift
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
IgM and IgD
lowest concentration
43. What cytokines to Th2 secrete?
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
IL 4 - 5 - 10 - 6
B - T - and NK cells
Local infection/inflammation; infection of the ln itself; metastasis
44. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Activate macrophages
Antimicrosomal and antithyroglobulin
The igA found in breast milk
45. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
T cell dysfunction
Tetanus - Botulinum - HBV - Rabies
The igA found in breast milk
46. Leukocyte adhesion defect presents with...
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
neutrophilia!
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
Antimicrosomal and antithyroglobulin
47. Describe the Mannose Lectin pathway
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
48. What is oprelevkin? and What is it used for?
...
Recom IL 11; thrombocytopenia
Anti TSh receptor
A - B - C; all the D's
49. The MALT/GALT are not...
Yes
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
encapsulated
Anti topoisomerase
50. What are the three types of lymphocytes?
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
B - T - and NK cells
Negative!
IgE; by activating eosinophils