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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.
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 duodenum - jejunum?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
T cell dysfunction
IgM
Superior mesenteric

2. What links the adaptive and innate immunity?
Kill them because they have CD16 on them that recognize the FcG portion
MHC I; from RER with help of the B2 microglobulin
Sinusitis - otitis media - pneumonia
Complement activation (active in both)

3. Only the _______ contribute to the Fc region
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
heavy chains

4. How is i Th1 helper cell inhibited?
Acts as second signal on B cells to induce class switching to IgE and IgG
Cytokine IL 10 secreted by Th2
T
Kill them because they have CD16 on them that recognize the FcG portion

5. 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).
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

6. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anti U1 RNP (ribonucleoprotein)
MHC I; from RER with help of the B2 microglobulin

7. What is the receptor for EBV? On what cells is that located?
Severe pyogenic infections early in life
pathogenesis
IL 3; supports growth and differentiation of bone marrow stem cells
CD21 on B cells (although there is T cell lymphocytosis in EBV)

8. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
MHC class molecules bind to KIRS or CD94 to prevent killing
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

9. What are MHC's necessary for? By themselves?
Anti SS- A (anti RO) and Anti SS- B
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T cell activation; no with CD 4 or CD 8

10. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
A chemotactic factor for neutrophils

11. What are the mediators that mast cells release?
All MHC 1/CD8
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Paracortex
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

12. what mediates the type II hypersensitivity? What are the two different methods?
RNA segment reassortment
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti Ach receptor
Antibody mediated cytotoxicity; either complement dependent or complement independent

13. What is three common causes of severe combined immunodef? What is the result of all three?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
IgA

14. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
acute phase reactants
Superficial inguinal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
2 heavy chains and two light chains

15. Leukocyte adhesion defect presents with...
...
neutrophilia!
pentamer
Antidesmoglein

16. what characterizes an arthus reaction?
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
Edema and necrosis in that region
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Activate macrophages

17. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Anti U1 RNP (ribonucleoprotein)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
MHC I - CD16 - CD56

18. Which MHC presents intracellular peptides? how so?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
MHC I; from RER with help of the B2 microglobulin
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Receiving preformed Antibodies

19. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
No because no peptide fragment!
Previous transfusion; pregnant woman whose fetus had paternal antigens
Type IV

20. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Antimicrosomal and antithyroglobulin
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

21. What is the general structure of an Ab?
Activates cytotoxic CD 8 T cells as second signal
2 heavy chains and two light chains
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
IL 5

22. What is the pathogenesis of a candida skin test?
Cyclosporine - OKT3
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Delayed type hypersensitivity

23. Which type of selection of thymic development provides central tolerance?
encapsulated
IL 4
Negative selection
MHC I - CD16 - CD56

24. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Superior mesenteric
Axillary

25. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti IF

26. __________ are a part of the innate system.
Acts as second signal on B cells to induce class switching to IgE and IgG
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
NK cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

27. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Antihistone
Previous transfusion; pregnant woman whose fetus had paternal antigens

28. From where do cytokines come from?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Lymphocytes
Bind FcG for antibody dependent cellular cytotoxicity
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

29. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Pernicious Anemia and Hashimotos
Thrombocytopenia
SP infections
Activate macrophages

30. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

31. The MALT/GALT are not...
encapsulated
IgM and IgA
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Local infection/inflammation; infection of the ln itself; metastasis

32. where do somatic hypermutation and class switching occur?
Inferior mesenteric
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
In the germinal center of secondary follicles (In the paler center)

33. where do NK cells develop?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Not thymus - BM
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Stimulate the liver to release acute phase reactants

34. Describe the capsular structure of a lymph node; What are the functions of the LN?
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 :(
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
Axillary
CD21 on B cells (although there is T cell lymphocytosis in EBV)

35. What are the autoantibodies for hashimotos?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 4
Antimicrosomal and antithyroglobulin

36. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
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
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 IgE and IgG

37. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Chronic granulomatous disease
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
pale central germinal centers

38. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Rheumatic arthritis
Paracortex
Lymphocytes

39. What does IL 4 do?
Paracortex
In the germinal center of secondary follicles (In the paler center)
Acts as second signal on B cells to induce class switching to IgE and IgG
Edema and necrosis in that region

40. What are the symptoms of serum sickness?
A - B - C; all the D's
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

41. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
secondary
Active; passive - fast but short half life (3 weeks!)
pale central germinal centers

42. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Paracortex; viral infection
Hereditary angioedema; PNH
Kill them because they have CD16 on them that recognize the FcG portion

43. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Anti topoisomerase
Remove encapsulated bacateria
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

44. What are the main symptoms of B cell immunodeficiencies?
IgA
SP infections
When you select for which MHC it will have; take out the lymphs that self react
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

45. What is the clinical use of Muromonab?
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
DM type I
IgG
Immunosuppression after kidney transplantation

46. What are the autoantibodies for primary biliary cirrhosis?
Interferon gamma; Th1
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anti mitochondrial

47. What is passive immunity?
Receiving preformed Antibodies
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
T cell precursor

48. The Fc region is found on the...
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
NK cells
carboxy terminal
Humoral

49. What are the two signals to kill for NK cells?
Anti Ach receptor
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Humoral

50. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Anti TSh receptor
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IL 1 and IL 6