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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. IgM can fix complement but...
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
cannot cross placenta
Recom IL 11; thrombocytopenia
Cells that stil have weird parts of their membrane that macrophages usually bite off

2. What bugs can actually infect the lymph node itself?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

3. How is i Th1 helper cell inhibited?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 4 - 5 - 10 - 6
Cytokine IL 10 secreted by Th2
Lymphocytes

4. For which toxins are preformed antibodies (passive) given?
Interferon gamma; Th1
Tetanus - Botulinum - HBV - Rabies
isotype
Anti IF

5. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Glycoproteins; HLA
Recom IL 11; thrombocytopenia
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

6. What is the main cytokine released by T cells? What does it do
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Para aortic
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IL 3; supports growth and differentiation of bone marrow stem cells

7. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
2 heavy chains and two light chains
Kill them because they have CD16 on them that recognize the FcG portion
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgG

8. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cytokine IL 10 secreted by Th2
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!
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

9. In general What are T cells good for?
Inferior mesenteric
Anti viral and anti tumor
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
IL 5

10. Name two endogenous pyrogens
Secretory component
Axillary
IL 1 and IL 6
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

11. What are the autoantibodies for myasthenia gravis?
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
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
Anti Ach receptor
Basophils! THey want IG E class switch!

12. What are the cell surface proteins on NK cells?
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
Anti topoisomerase
MHC I - CD16 - CD56
Immunoflourescent staining of tissue biopsies

13. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

14. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Macrophages - Dendritic cells - B cells
Recom IL 11; thrombocytopenia
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

15. where do somatic hypermutation and class switching occur?
Tetanus - Botulinum - HBV - Rabies
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
In the germinal center of secondary follicles (In the paler center)

16. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
All MHC 1/CD8
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
C5a

17. T/F B cells do not require a second signal
Th cells fail to produce interferon gamma; a lot of IgE
heavy chains
IgM and IgD
False! B cell class switching requires a second signal

18. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgG
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 :(

19. How does complement link innate and adaptive?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Macrophages - Dendritic cells - B cells
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

20. what cell surface proteins are on all APCs?
not Ab mediated
Celiac
dimer
MHC II - B7

21. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Axillary
Fc

22. What does IL 5 do?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
carboxy terminal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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

23. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
MHC I; from RER with help of the B2 microglobulin
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

24. What are the two signals required for T cells? what happens after?
except hyperacute
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Acts as second signal on B cells to induce class switching to IgE and IgG
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

25. What are the autoantibodies for type I diabetes mellitus?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti glutamate carboxylase and anti insulin

26. What does interferon gamma do to be antiviral?
Remove encapsulated bacateria
Increases expression of MHC I and MHC II and also activates NK cells
MHC II - B7
Active; passive - fast but short half life (3 weeks!)

27. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
MHC class molecules bind to KIRS or CD94 to prevent killing
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
Kill them because they have CD16 on them that recognize the FcG portion
If there is class switching and plasma cell production (that is when memory cells are produced)

28. What is the common variable immunodeficiency ? How is it different from Brutons?
Acts as second signal on B cells to induce class switching to IgE and IgG
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
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

29. What lymph node drains the lateral side of the dorsum of the foot?
IL 15; IL 12 - interferon Beta and interferon alpha
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
Popliteal
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

30. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Anti Ach receptor
...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

31. Complements are...
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
acute phase reactants
Sinusitis - otitis media - pneumonia
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

32. What is the autoantibody for SLE that is nonspecific? Specific?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

33. The MALT/GALT are not...
Anti mitochondrial
Delayed type hypersensitivity
By transcytosis
encapsulated

34. What are superantigens? give two examples.
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Liver! (they are proteins circulating in the blood)

35. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
active complement pathway
All MHC 1/CD8
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

36. How is the thymus organized? what happens in each section?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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

37. give an example of how influenza does a major antigenic shift.
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
RNA segment reassortment
Immunoflourescent staining of tissue biopsies
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

38. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti IF
Superficial inguinal

39. The Fc region is found on the...
Negative selection
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
carboxy terminal

40. The secondary follicles have __________; primary follicles are dense
Remove encapsulated bacateria
The patient could become cyanotic in the OR!
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
pale central germinal centers

41. Which helper T cells' development is induced by IL 4? IL 12?
Bind FcG for antibody dependent cellular cytotoxicity
Th2; Th1
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

42. To what portion of the Antibody do the complements bind?
Fc
CD56
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
In the germinal center of secondary follicles (In the paler center)

43. What do mature naive B lymphocytes express?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
The patient could become cyanotic in the OR!
IgM and IgD
mesenchymal

44. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
Daclizumab; prevent ACUTE rejection of renal transplant
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Pernicious Anemia and Hashimotos

45. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Yes
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
MS - hay fever - SLE - goodpastures
Cytokine IL 10 secreted by Th2

46. which antibody activate mast cells - basophils - and eosinophils?
Paracortex; viral infection
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Pernicious Anemia and Hashimotos
IgE

47. What are the autoantibodies for autoimmune hepatitis?
not Ab mediated
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anti smooth muscle

48. Which MHC presents intracellular peptides? how so?
MHC II - B7
S. aureus - E. Coli - aspergillus
lowest concentration
MHC I; from RER with help of the B2 microglobulin

49. Monomer in circulation - ___ when secreted
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
Recom IL 11; thrombocytopenia
dimer
A j chain

50. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
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
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
Superficial inguinal

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USMLE Step 1 Immunology

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