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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 antibody mediates immunity to worms? how?
Liver! (they are proteins circulating in the blood)
Popliteal
Basophils! THey want IG E class switch!
IgE; by activating eosinophils

2. What is digoxin immune Fab used for?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Rheumatic arthritis
Cells that stil have weird parts of their membrane that macrophages usually bite off
Antidote for digoxin intoxication

3. What lymph node drains the scrotum?
Superficial inguinal
Barrel hoop basement membrane fenestrations
Anti viral and anti tumor
Antimicrosomal and antithyroglobulin

4. where do NK cells develop?
TGF beta and IL 10
MS
Not thymus - BM
Alternative splicing of mRNA

5. What is the main function of IL 12? other than macrophages who else can release IL 12?
Hemochromatosis
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgAs in mothers breast milk!

6. What do mature naive B lymphocytes express?
IL 1 and IL 6
IgM and IgD
IgE
Local infection/inflammation; infection of the ln itself; metastasis

7. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
MS
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

8. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 3; supports growth and differentiation of bone marrow stem cells
carboxy terminal

9. What are the autoantibodies for wegeners granulomatosis?
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
Basophils! THey want IG E class switch!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

10. How is the antigen loaded onto a MHC II?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
MHC II - B7

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

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12. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Bind FcG for antibody dependent cellular cytotoxicity
Activate macrophages
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/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

13. What lymph node drains the lateral side of the dorsum of the foot?
Thrombocytopenia
Popliteal
Edema and necrosis in that region
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

14. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Influenza; antigenic shift; antigenic drift
All MHC 1/CD8
Hereditary angioedema; PNH

15. What are the autoantibodies for Celiac disease?
Tetanus - Botulinum - HBV - Rabies
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

16. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
IL 4
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
except hyperacute

17. What is three common causes of severe combined immunodef? What is the result of all three?
DM type I
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Tetanus - Botulinum - HBV - Rabies

18. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Rheumatic arthritis
Bind FcG for antibody dependent cellular cytotoxicity
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

19. What does interferon gamma do? What two type of cells does it attack mostly?
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Superficial inguinal

20. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
MS
Secretory component

21. What are the T cell functions?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
By transcytosis
Severe pyogenic infections early in life
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

22. What are the autoantibodies for systemic sclerosis?
Activate macrophages
Barrel hoop basement membrane fenestrations
cannot cross placenta
Anti topoisomerase

23. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
B - T - and NK cells
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Local infection/inflammation; infection of the ln itself; metastasis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

24. What is the treatment of acute transplant rejection?
Type IV
Cyclosporine - OKT3
Superficial inguinal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

25. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

26. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Wiskott Aldrich syndrome
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

27. What is the pathogenesis of acute transplant rejection? When does it occur?
Superficial inguinal
DM type I
Yes
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

28. What are the autoantibodies for goodpastures syndrome?
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
Anti alpha subunit 3 of collagen on type IV bm
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti U1 RNP (ribonucleoprotein)

29. Only the _______ contribute to the Fc region
heavy chains
MHC I - CD16 - CD56
Antibody mediated cytotoxicity; either complement dependent or complement independent
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

30. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Basophils! THey want IG E class switch!

31. What is recomb beta interferon used for?
MS
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Inferior mesenteric
Remove encapsulated bacateria

32. The Fc region is found on the...
carboxy terminal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cytokine IL 10 secreted by Th2
DM type I

33. What lymph node drains the breast?
acute phase reactants
Internal iliac
Axillary
Fc

34. What is the white pulp of the spleen?
Thrombocytopenia
IgM
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgM and IgG

35. What is muromonab - CD3 (OKT3)
Its a serine protease that activates apoptosis; NK and CD8
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgA
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

36. what characterizes an arthus reaction?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Edema and necrosis in that region
Negative nitroblue tetrazolium reduction test
T cell dysfunction

37. Describe complement dependent Type II hypersensitivity. Give an example.
Daclizumab; prevent ACUTE rejection of renal transplant
MHC II - B7
Antihistone
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A

38. What is the main cytokine that activates eosinophils?
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
IL 5
If there is class switching and plasma cell production (that is when memory cells are produced)
Influenza; antigenic shift; antigenic drift

39. What is chronic mucocutaneous candidiasis d/t?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Activate macrophages
IL 1 and IL 6
T cell dysfunction

40. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
MHC I; from RER with help of the B2 microglobulin
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! 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!

41. What are the autoantibodies for hashimotos?
IL 5
pathogenesis
Sinusitis - otitis media - pneumonia
Antimicrosomal and antithyroglobulin

42. 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
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
Antidote for digoxin intoxication
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

43. What is filgrastim and sargramostim? and What is it used for?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Inferior mesenteric
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

44. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
All MHC 1/CD8
T
encapsulated

45. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
heavy chains
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

46. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
Recom IL 11; thrombocytopenia
Not thymus - BM
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

47. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Pernicious Anemia and Hashimotos
Paracortex
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Its a serine protease that activates apoptosis; NK and CD8

48. What are the function of B 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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

49. IgG...
IL 3; supports growth and differentiation of bone marrow stem cells
Carbohydrate
Basophils! THey want IG E class switch!
opsonizes

50. hat is the presentation of Jobs syndrome or Hyper IgE?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
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
C5a
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)