Test your basic knowledge |

USMLE Step 1 Immunology

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 type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Anti smooth muscle
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
When you select for which MHC it will have; take out the lymphs that self react
Bind FcG for antibody dependent cellular cytotoxicity

2. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
TNF alpha and IL1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Receiving preformed Antibodies

3. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
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
Complement activation (active in both)
MS

4. What lymph node drains the duodenum - jejunum?
Th2; Th1
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
mesenchymal
Superior mesenteric

5. Which is the most abundant antibody in blood?
Interferon gamma; Th1
IL 4 - 5 - 10 - 6
IgG
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

6. which antibodies prevent antigens from binding mucosal surfaces?
Immunoflourescent staining of tissue biopsies
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgA
opsonizes

7. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
type four
pentamer
cannot cross placenta

8. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
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

9. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti smooth muscle

10. What does interferon gamma do? What two type of cells does it attack mostly?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
pathogenesis
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

11. What are the autoantibodies for type I diabetes mellitus?
Paracortex
Anti glutamate carboxylase and anti insulin
Antihistone
SP infections

12. What is the pathology seen in chronic transplant rejection?
Daclizumab; prevent ACUTE rejection of renal transplant
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti smooth muscle
MHC II - B7

13. What are the symptoms of serum sickness?
MHC II - B7
T cell precursor
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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

14. The ______ in the BM are DN - the DP are in the cortex of thymus
encapsulated
delayed!
T cell precursor
Anti mitochondrial

15. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
IL 5
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

16. What is the white pulp of the spleen?
Chronic granulomatous disease
Axillary
T
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

17. which of the hypersensitivity reactions is not Ab mediated?
Type IV
C5a
Barrel hoop basement membrane fenestrations
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

18. 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?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
All MHC 1/CD8
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
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

19. 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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Bind FcG for antibody dependent cellular cytotoxicity
Viral neutralization of igM and IgG!

20. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Kill them because they have CD16 on them that recognize the FcG portion
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 :(
...
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

21. Name two endogenous pyrogens
Cells that stil have weird parts of their membrane that macrophages usually bite off
IL 1 and IL 6
In the germinal center of secondary follicles (In the paler center)
isotype

22. What lymph node drains the stomach?
Type IV
Celiac
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

23. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

24. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC class molecules bind to KIRS or CD94 to prevent killing
Antimicrosomal and antithyroglobulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

25. What are target cells?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Barrel hoop basement membrane fenestrations
lowest concentration
Cells that stil have weird parts of their membrane that macrophages usually bite off

26. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
C5a
Anti viral and anti tumor

27. What is recomb beta interferon used for?
MS
dimer
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
Anti topoisomerase

28. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Increases expression of MHC I and MHC II and also activates NK cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
acute phase reactants

29. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Liver! (they are proteins circulating in the blood)
Yes
Celiac

30. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
Axillary

31. How does the alternative pathway lead to MAC activation?
Activates Th1 helper cells; Macrophages
encapsulated
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
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

32. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Anti mitochondrial
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
By transcytosis

33. What is the main cytokine that activates eosinophils?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
T cell precursor
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IL 5

34. other than mediating shock - what else does TNF alpha do? who releases it mainly?
TLR ad nuclear receptors
Activates Th1 helper cells; Macrophages
Superficial inguinal
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

35. What are the autoantibodies for myasthenia gravis?
CD56
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Tetanus - Botulinum - HBV - Rabies
Anti Ach receptor

36. What does granulysin do?
Inferior mesenteric
...
Anti SS- A (anti RO) and Anti SS- B
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

37. What happens in a deficiency of C3?
Kill them because they have CD16 on them that recognize the FcG portion
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Local infection/inflammation; infection of the ln itself; metastasis

38. 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?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
False! B cell class switching requires a second signal
Celiac

39. Which is the main antibody that provides passive immunity to infants?
By transcytosis
IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

40. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
IgAs in mothers breast milk!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

41. In thymic development - What is the positive selection? negative selections?
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
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
When you select for which MHC it will have; take out the lymphs that self react

42. What are the three types of APCs?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Macrophages - Dendritic cells - B cells
Complement activation (active in both)

43. What are the main symptoms of T cell immunodeficiencies?
IgG
Antihistone
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

44. What is thrombopoietin used for?
IgM and IgG
C5a
Th cells fail to produce interferon gamma; a lot of IgE
Thrombocytopenia

45. What does IL 2 do?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activates cytotoxic CD 8 T cells as second signal
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

46. What are the T cell functions?
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)
Activates Th1 helper cells; Macrophages
CRP - C3b - IgM
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

47. What is the pathogenesis of a hypersensitivity reaction?
In the germinal center of secondary follicles (In the paler center)
Receiving preformed Antibodies
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
Humoral

48. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Bind FcG for antibody dependent cellular cytotoxicity
Anti Ach receptor
Anemias (esp due to renal failure)
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

49. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Rheumatic arthritis
lowest concentration
Humoral

50. How does igA cross the epithelium?
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
By transcytosis
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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!