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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. The lymphocytes are ________ origin
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
mesenchymal
A chemotactic factor for neutrophils
TNF alpha and IL1

2. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation
If there is class switching and plasma cell production (that is when memory cells are produced)
Edema and necrosis in that region

3. what cell surface proteins are on all APCs?
MHC II - B7
Antimicrosomal and antithyroglobulin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Graves

4. What is recomb alpha interferon used for?
IL 3; supports growth and differentiation of bone marrow stem cells
A chemotactic factor for neutrophils
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

5. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Superior mesenteric
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

6. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Th cells fail to produce interferon gamma; a lot of IgE
False! B cell class switching requires a second signal

7. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Severe pyogenic infections early in life
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

8. What are the main cell surface proteins on B cells?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
delayed!

9. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC I - CD16 - CD56
Antihistone

10. Which diseases are associated with DR4?
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
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
DM type I and RA
MHC II - B7

11. What are the symptoms of serum sickness?
By transcytosis
isotype
cannot cross placenta
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

12. What are the autoantibodies for hashimotos?
Hemochromatosis
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
Receiving preformed Antibodies
Antimicrosomal and antithyroglobulin

13. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
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
Daclizumab; prevent ACUTE rejection of renal transplant
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Edema and necrosis in that region

14. From where do cytokines come from?
Lymphocytes
Humoral
Rheumatic arthritis
Influenza; antigenic shift; antigenic drift

15. which of the transplant rejections is antibody mediated? why does it occur?
Negative selection
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgAs in mothers breast milk!
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

16. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Viral neutralization of igM and IgG!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

17. What are the two signals required for Th1 cells? what happens after then activated?
Inferior mesenteric
Edema and necrosis in that region
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

18. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

19. what characterizes an arthus reaction?
Carbohydrate
Fab portion
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Edema and necrosis in that region

20. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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!
DM type I
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

21. What does IL 4 do?
T cell dysfunction
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Lymphocytes

22. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
B - T - and NK cells
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

23. What is the most common selective Ig deficiency? What is the presentation?
IgE
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

24. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Chronic granulomatous disease
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
heavy chains

25. What are the main symptoms of B cell immunodeficiencies?
IL 15; IL 12 - interferon Beta and interferon alpha
SP infections
not Ab mediated
Chronic granulomatous disease

26. Which antibodies can be multimeric?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Its a serine protease that activates apoptosis; NK and CD8
IgM and IgA
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

27. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Antimicrosomal and antithyroglobulin
Inferior mesenteric
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

28. What is the toxicity of azathioprine?
Sinusitis - otitis media - pneumonia
Influenza; antigenic shift; antigenic drift
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
...

29. What are the autoantibodies for Celiac disease?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
...
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

30. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
Anti mitochondrial
Delayed type hypersensitivity
Superficial inguinal

31. What is colostrum?
Severe pyogenic infections early in life
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
The igA found in breast milk
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 :(

32. Which antibody mediates immunity to worms? how?
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 :(
IgE; by activating eosinophils
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

33. which antibodies can bind complement?
Kill them because they have CD16 on them that recognize the FcG portion
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
IgM and IgG
active complement pathway

34. How is sirolimus different from tacrolimus?
Stimulate the liver to release acute phase reactants
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
carboxy terminal
Anti glutamate carboxylase and anti insulin

35. What is the autoantibody for SLE that is nonspecific? Specific?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti alpha subunit 3 of collagen on type IV bm
isotype
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

36. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

37. Which disease is associated with HLA A3?
pentamer
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Hemochromatosis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

38. Which HLA's are included in MHC I? MHC II?

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39. what prevents NK cells from killing normal cells if their default is to kill?
except hyperacute
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
MHC class molecules bind to KIRS or CD94 to prevent killing

40. IgM can fix complement but...
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
cannot cross placenta

41. The secondary follicles have __________; primary follicles are dense
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
pale central germinal centers
Antibody mediated cytotoxicity; either complement dependent or complement independent

42. What is the presentation of hyperIgM syndrome?
IgM and IgG
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Severe pyogenic infections early in life

43. What is the mechanism for sirolimus? what else it known as?
Severe pyogenic infections early in life
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
Anti IF
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

44. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Type IV
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Acts as second signal on B cells to induce class switching to IgE and IgG

45. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
isotype
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
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

46. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
SP infections
MHC I - CD16 - CD56

47. __________ are a part of the innate system.
Chronic granulomatous disease
A chemotactic factor for neutrophils
NK cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

48. which antibody is involved in the primary response or immediate response to an antigen?
Cytokine IL 10 secreted by Th2
DM type I and RA
IgM
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

49. So antibodies are the effectors for the humoral response. List some of their functions.
TNF alpha and IL1
IgE
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

50. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Celiac