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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. IgM can fix complement but...
cannot cross placenta
If there is class switching and plasma cell production (that is when memory cells are produced)
Glycoproteins; HLA
Interferon gamma; Th1

2. which antibodies can bind complement?
IgM and IgG
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

3. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Immunosuppression after kidney transplantation

4. Which diseases are associated with DR5?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Pernicious Anemia and Hashimotos
TNF alpha and IL1
Antihistone

5. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Increases expression of MHC I and MHC II and also activates NK cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

6. What are the labs in brutons agammaglobulinemia?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
opsonizes
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Alternative splicing of mRNA

7. What do mature naive B lymphocytes express?
IgM and IgD
Macrophages - Dendritic cells - B cells
Negative nitroblue tetrazolium reduction test
Para aortic

8. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Kill them because they have CD16 on them that recognize the FcG portion
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IL 3; supports growth and differentiation of bone marrow stem cells

9. What are the autoantibodies for Celiac disease?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
pale central germinal centers
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

10. What is the main cytokine that activates eosinophils?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 5
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 :(

11. Complements are...
acute phase reactants
In the germinal center of secondary follicles (In the paler center)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgAs in mothers breast milk!

12. To what portion of the Antibody do the complements bind?
Fc
Anti Ach receptor
Alternative splicing of mRNA
Paracortex

13. What is the main cytokine released by T cells? What does it do
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IL 3; supports growth and differentiation of bone marrow stem cells

14. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
A chemotactic factor for neutrophils
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
Receiving preformed Antibodies

15. What are some catalase positive organisms?
A recomb cytokine of IL 2; RCC and metastatic melanoma
S. aureus - E. Coli - aspergillus
MHC II - B7
Tetanus - Botulinum - HBV - Rabies

16. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Superior mesenteric
Stimulate the liver to release acute phase reactants
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

17. What is the pathogenesis of a candida skin test?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Delayed type hypersensitivity
Hemochromatosis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

18. Leukocyte adhesion defect presents with...
neutrophilia!
Activate macrophages
IgM and IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

19. What is the main function of IL 8?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Carbohydrate
A chemotactic factor for neutrophils
By transcytosis

20. In general What are T cells good for?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti viral and anti tumor
Basophils! THey want IG E class switch!
Antibody mediated cytotoxicity; either complement dependent or complement independent

21. What are superantigens? give two examples.
Barrel hoop basement membrane fenestrations
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
T

22. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
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
Activate macrophages
IL 4 - 5 - 10 - 6

23. What does IL 10 do? who is secreted by?
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
Rheumatic arthritis
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
All MHC 1/CD8

24. What are the autoantibodies for myasthenia gravis?
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
Steroid responsive nephrotic syndrome
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti Ach receptor

25. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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

26. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Superficial inguinal
Kill them because they have CD16 on them that recognize the FcG portion
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

27. What is the mechanism for sirolimus? what else it known as?
Th cells fail to produce interferon gamma; a lot of IgE
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
Paracortex; viral infection
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

28. What are the autoantibodies for systemic sclerosis?
Steroid responsive nephrotic syndrome
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti topoisomerase
IgE

29. The Fc region is found on the...
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
carboxy terminal
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti U1 RNP (ribonucleoprotein)

30. How is sirolimus different from tacrolimus?
Cross link
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
RNA segment reassortment
Pernicious Anemia and Hashimotos

31. What lymph node drains the scrotum?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Local infection/inflammation; infection of the ln itself; metastasis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Superficial inguinal

32. What are the autoantibodies for graves?
Negative!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti TSh receptor
lowest concentration

33. Which disease is associated withB B27?
heavy chains
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Superficial inguinal
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

34. What does IL 5 do?
SP infections
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
Sinusitis - otitis media - pneumonia
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

35. What is epo used for?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anemias (esp due to renal failure)
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

36. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
IgE
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgM
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

37. What is chronic mucocutaneous candidiasis d/t?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
T cell dysfunction
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

38. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
Pernicious Anemia and Hashimotos
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)

39. What is the treatment of acute transplant rejection?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cyclosporine - OKT3
TGF beta and IL 10
False! B cell class switching requires a second signal

40. What is the pathogenesis of HyperIgE syndrome? What are the labs?
isotype
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
A chemotactic factor for neutrophils
Th cells fail to produce interferon gamma; a lot of IgE

41. What are the main cell surface proteins on B cells?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Superior mesenteric

42. What is a factor that is a predictor for a bad transplantation?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Paracortex; viral infection
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

43. What is recomb gamma interferon used for?
Rheumatic arthritis
C5a
Chronic granulomatous disease
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

44. What cytokines are released by Th1 cells?
Previous transfusion; pregnant woman whose fetus had paternal antigens
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Interferon gamma and IL 2

45. 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?
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Steroid responsive nephrotic syndrome
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

46. How does igA cross the epithelium?
By transcytosis
B - T - and NK cells
Kill them because they have CD16 on them that recognize the FcG portion
MS

47. What are the autoantibodies for pemphigus bulgaris?
Superficial inguinal
pathogenesis
Antidesmoglein
A j chain

48. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Yes

49. The MALT/GALT are not...
encapsulated
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
A recomb cytokine of IL 2; RCC and metastatic melanoma
Secretory component

50. which interleukin receptor is required for NK development? activation?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
IL 15; IL 12 - interferon Beta and interferon alpha
Daclizumab; prevent ACUTE rejection of renal transplant

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USMLE Step 1 Immunology

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