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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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 of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
MHC class molecules bind to KIRS or CD94 to prevent killing
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antibody mediated cytotoxicity; either complement dependent or complement independent
Chronic granulomatous disease

2. What is recomb gamma interferon used for?
Chronic granulomatous disease
Anti topoisomerase
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
Barrel hoop basement membrane fenestrations

3. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
MS - hay fever - SLE - goodpastures
B - T - and NK cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Cross link

4. What is the presentation of Brutons agammaglobulinemia?
Pernicious Anemia and Hashimotos
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Negative nitroblue tetrazolium reduction test

5. What are the labs in brutons agammaglobulinemia?
IL 4 - 5 - 10 - 6
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
pentamer

6. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
secondary
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Macrophages - Dendritic cells - B cells

7. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Cytokine IL 10 secreted by Th2
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
A chemotactic factor for neutrophils

8. What is the clinical use for sirolimus? what should you combine it with?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lymphocytes
Inferior mesenteric

9. 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?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Th2; Th1
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
IgG

10. How is sirolimus different from tacrolimus?
Its main effect is a defect in Ab opsonization for killing
Carbohydrate
Activates cytotoxic CD 8 T cells as second signal
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

11. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Anti alpha subunit 3 of collagen on type IV bm
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

12. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Antidote for digoxin intoxication

13. What is oprelevkin? and What is it used for?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
...
Negative nitroblue tetrazolium reduction test
Recom IL 11; thrombocytopenia

14. What is the main function of IL 8?
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
Kill them because they have CD16 on them that recognize the FcG portion
A chemotactic factor for neutrophils
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

15. What is anergy? why does this occur?
IgM and IgD
carboxy terminal
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Carbohydrate

16. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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

17. The two heavy chains of an antibody contribute to the...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Interferon gamma and IL 2
Fab portion

18. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Kill them because they have CD16 on them that recognize the FcG portion
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Viral neutralization of igM and IgG!
Influenza; antigenic shift; antigenic drift

19. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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

20. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Immunosuppression after kidney transplantation
Popliteal
Anti Ach receptor

21. What lymph node drains the duodenum - jejunum?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Superior mesenteric

22. 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?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

23. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
False! B cell class switching requires a second signal
When you select for which MHC it will have; take out the lymphs that self react
cannot cross placenta

24. What lymph node drains the upper limb?
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
Axillary
Anti SS- A (anti RO) and Anti SS- B
The igA found in breast milk

25. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Previous transfusion; pregnant woman whose fetus had paternal antigens
heavy chains
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

26. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
IL 4 - 5 - 10 - 6
MS
Superficial inguinal

27. What type of side chains are found on Fc region of an antibody?
Popliteal
Carbohydrate
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superior mesenteric

28. What is the presentation of hyperIgM syndrome?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
When you select for which MHC it will have; take out the lymphs that self react
Severe pyogenic infections early in life

29. What happens in a deficiency of C3?
MHC I; from RER with help of the B2 microglobulin
Fc
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

30. What lymph node drains the testes?
IL 1 and IL 6
CD56
Para aortic
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

31. when can graft versus host disease? What is the result?
Wiskott Aldrich syndrome
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
neutrophilia!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Chronic granulomatous disease
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
encapsulated

33. 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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
TNF alpha and IL1

34. What is the clinical use for azathioprine?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Viral neutralization of igM and IgG!
...

35. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
acute phase reactants
Cross link
Anti IF

36. __________ are a part of the innate system.
NK cells
Anemias (esp due to renal failure)
Cross link
Cyclosporine - OKT3

37. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
A recomb cytokine of IL 2; RCC and metastatic melanoma
Immunosuppression after kidney transplantation
IgE

38. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Fc
delayed!
except hyperacute
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

39. what cytokine does basophils secrete?
Inferior mesenteric
IL 4
Anti smooth muscle
IgM and IgA

40. Which diseases are associated with DR2?
T cell precursor
MS - hay fever - SLE - goodpastures
Rheumatic arthritis
RNA segment reassortment

41. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
MHC I; from RER with help of the B2 microglobulin
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

42. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Secretory component
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
Complement activation (active in both)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

43. 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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

44. What links the adaptive and innate immunity?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
CRP - C3b - IgM
Complement activation (active in both)
Kill them because they have CD16 on them that recognize the FcG portion

45. The Fc region is found on the...
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Pernicious Anemia and Hashimotos
carboxy terminal
cannot cross placenta

46. What is thrombopoietin used for?
Interferon gamma and IL 2
Thrombocytopenia
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
C5a

47. How does complement link innate and adaptive?
If there is class switching and plasma cell production (that is when memory cells are produced)
Edema and necrosis in that region
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

48. What are the function of B cells?
IgA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Anti SS- A (anti RO) and Anti SS- B
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

49. Which diseases are associated with DR4?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Bind FcG for antibody dependent cellular cytotoxicity
DM type I and RA

50. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
SP infections
encapsulated
T