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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What are the T cell functions?
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
MS

2. Describe the Mannose Lectin pathway
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
IL 15; IL 12 - interferon Beta and interferon alpha
Severe pyogenic infections early in life
Th2; Th1

3. What lymph node drains the thigh?
Superficial inguinal
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IL 5
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

4. The Fc region is found on the...
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
carboxy terminal
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

5. which B and T cell disorder presents with specifically low IgM?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Wiskott Aldrich syndrome
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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

6. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Cytokine IL 10 secreted by Th2
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

7. The two heavy chains of an antibody contribute to the...
Anti glutamate carboxylase and anti insulin
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Fab portion
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

8. What are the autoantibodies for wegeners granulomatosis?
Popliteal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

9. What lymph node drains the duodenum - jejunum?
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
Superior mesenteric
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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

10. What are the labs in brutons agammaglobulinemia?
In the germinal center of secondary follicles (In the paler center)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

11. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Bind FcG for antibody dependent cellular cytotoxicity
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
mesenchymal

12. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
neutrophilia!
MHC class molecules bind to KIRS or CD94 to prevent killing

13. What is the most common selective Ig deficiency? What is the presentation?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Popliteal
dimer

14. what cell surface proteins are on all APCs?
MHC II - B7
MHC class molecules bind to KIRS or CD94 to prevent killing
T cell dysfunction
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

15. which of the hypersensitivity reactions is not Ab mediated?
Negative nitroblue tetrazolium reduction test
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
CD56
Type IV

16. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anemias (esp due to renal failure)
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

17. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
IgM and IgD
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 :(

18. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Alternative splicing of mRNA
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

19. A lymph node is a ________ lymphoid organ.
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
pentamer
Anti Jo -1
secondary

20. what prevents NK cells from killing normal cells if their default is to kill?
Inferior mesenteric
Anti alpha subunit 3 of collagen on type IV bm
MHC class molecules bind to KIRS or CD94 to prevent killing
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

21. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Activates Th1 helper cells; Macrophages
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
False! B cell class switching requires a second signal
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

22. How is the antigen loaded onto a MHC II?
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Wiskott Aldrich syndrome

23. How does igA cross the epithelium?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
By transcytosis
IL 15; IL 12 - interferon Beta and interferon alpha

24. What are the two signals required for B cell class switching? Which is the second signal?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti Jo -1

25. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
not Ab mediated
Interferon gamma; Th1
Cyclosporine - OKT3
pathogenesis

26. What is serum sickness? give an example.
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
Axillary
isotype
MHC class molecules bind to KIRS or CD94 to prevent killing

27. What are the PALS?
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
Activates cytotoxic CD 8 T cells as second signal
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

28. IgE has the ___________ in the serum
except hyperacute
Fab portion
lowest concentration
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

29. What is the presentation of Brutons agammaglobulinemia?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

30. The lymphocytes are ________ origin
In the germinal center of secondary follicles (In the paler center)
Anti alpha subunit 3 of collagen on type IV bm
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
mesenchymal

31. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM and IgD
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anemias (esp due to renal failure)

32. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Viral neutralization of igM and IgG!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Superficial inguinal

33. Which MHC presents intracellular peptides? how so?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Severe pyogenic infections early in life
MHC I; from RER with help of the B2 microglobulin
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

34. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
T cell dysfunction
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
mesenchymal

35. What happens in a secondary follicle?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Previous transfusion; pregnant woman whose fetus had paternal antigens
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

36. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Viral neutralization of igM and IgG!
DM type I
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
T cell dysfunction

37. which cells have more complete tolerance - B or T cells?
T
Its main effect is a defect in Ab opsonization for killing
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
CRP - C3b - IgM

38. What are C1 - C2 - C3 - C4 important for?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Viral neutralization of igM and IgG!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antidote for digoxin intoxication

39. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
False! B cell class switching requires a second signal
MS
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

40. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Type IV

41. What lymph node drains the anal canal (below the pectinate line)?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Superficial inguinal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Sinusitis - otitis media - pneumonia

42. which antibodies prevent antigens from binding mucosal surfaces?
IgA
The igA found in breast milk
Complement activation (active in both)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

43. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A chemotactic factor for neutrophils
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
delayed!

44. What lymph node drains the rectum (above the pectinate line)?
IgG
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Internal iliac
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

45. What are the three types of lymphocytes?
S. aureus - E. Coli - aspergillus
not Ab mediated
IgG
B - T - and NK cells

46. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Secretory component

47. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Edema and necrosis in that region
Anti glutamate carboxylase and anti insulin
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!

48. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
...
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

49. Which antibody mediates immunity to worms? how?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IgE; by activating eosinophils
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IgE

50. What does Interferon alpha and beta do? how?
TLR ad nuclear receptors
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

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USMLE Step 1 Immunology

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