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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. What is the main function of IL 12? other than macrophages who else can release IL 12?
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
Axillary
Anemias (esp due to renal failure)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

2. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Th2; Th1
Superficial inguinal
Internal iliac
except hyperacute

3. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
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)
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!
Local infection/inflammation; infection of the ln itself; metastasis

4. What is the treatment of acute transplant rejection?
Para aortic
IL 15; IL 12 - interferon Beta and interferon alpha
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Cyclosporine - OKT3

5. What cytokines to Th2 secrete?
Humoral
IL 4 - 5 - 10 - 6
Receiving preformed Antibodies
TGF beta and IL 10

6. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Paracortex
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Activates Th1 helper cells; Macrophages

7. which B and T cell disorder presents with specifically low IgM?
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
Th2; Th1
Wiskott Aldrich syndrome
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

8. What links the adaptive and innate immunity?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Complement activation (active in both)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

9. What do multimeric antibodies require for assembly?
T
A j chain
All MHC 1/CD8
2 heavy chains and two light chains

10. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
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
isotype
active complement pathway

11. IgM can exist as a _______ also
pentamer
Humoral
Pernicious Anemia and Hashimotos
No because no peptide fragment!

12. what cytokine does basophils secrete?
Inferior mesenteric
Viral neutralization of igM and IgG!
All MHC 1/CD8
IL 4

13. 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?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
secondary
Edema and necrosis in that region
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

14. What do mature naive B lymphocytes express?
IgM and IgD
Popliteal
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
Negative selection

15. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Humoral
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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

16. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Histamine; post capillary venules - vasodilation
T cell dysfunction
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
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

17. What lymph node drains the upper limb?
Axillary
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti U1 RNP (ribonucleoprotein)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

18. What are the autoantibodies for hashimotos?
active complement pathway
Anti SS- A (anti RO) and Anti SS- B
Antimicrosomal and antithyroglobulin
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

19. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
T cell precursor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 4
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 :(

20. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Yes
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

21. Which are the only two antiinflammatory cytokines?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
TGF beta and IL 10
CD56
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

22. what secretes IL 4?
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
Stimulate the liver to release acute phase reactants
Graves
Basophils! THey want IG E class switch!

23. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Th2; Th1

24. What does IL 5 do?
Anti U1 RNP (ribonucleoprotein)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Histamine; post capillary venules - vasodilation
TNF alpha and IL1

25. What is three common causes of severe combined immunodef? What is the result of all three?
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
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Active; passive - fast but short half life (3 weeks!)

26. which type of immunity is slow but long lasting? as opposed to...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Active; passive - fast but short half life (3 weeks!)

27. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Cyclosporine - OKT3
T cell dysfunction

28. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Kill them because they have CD16 on them that recognize the FcG portion
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

29. What is the defect in hyper IgM syndrome? What are the lab results?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti Ach receptor

30. How does the alternative pathway lead to MAC activation?
delayed!
Barrel hoop basement membrane fenestrations
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
Axillary

31. What is the toxicity of azathioprine?
Secretory component
...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

32. What is the pathogenesis of a hypersensitivity reaction?
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
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
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
Hereditary angioedema; PNH

33. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
TGF beta and IL 10

34. What are the main symptoms of B cell immunodeficiencies?
SP infections
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MHC class molecules bind to KIRS or CD94 to prevent killing
Glycoproteins; HLA

35. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
MHC I; from RER with help of the B2 microglobulin
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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

36. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Increases expression of MHC I and MHC II and also activates NK cells
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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

37. What are the T cell functions?
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
No because no peptide fragment!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

38. Which disease is associated with DR7?
Alternative splicing of mRNA
Steroid responsive nephrotic syndrome
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

39. How does complement link innate and adaptive?
Increases expression of MHC I and MHC II and also activates NK cells
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Graves
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

40. The MALT/GALT are not...
IgM
encapsulated
secondary
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

41. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
dimer
neutrophilia!
Its a serine protease that activates apoptosis; NK and CD8

42. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
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

43. What is the presentation of Brutons agammaglobulinemia?
IgG
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Superior mesenteric

44. What is the main function of TNF alpha? How does it do this?
Steroid responsive nephrotic syndrome
MHC I; from RER with help of the B2 microglobulin
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

45. What is passive immunity?
Receiving preformed Antibodies
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

46. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
DM type I and RA
Histamine; post capillary venules - vasodilation
Influenza; antigenic shift; antigenic drift

47. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
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
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

48. What are the autoantibodies for other vasculitides?
DM type I
IL 15; IL 12 - interferon Beta and interferon alpha
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

49. T/F B cells do not require a second signal
Immunoflourescent staining of tissue biopsies
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
False! B cell class switching requires a second signal
Graves

50. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
cannot cross placenta
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
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