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tsomkapQ > Immunology > Flashcards

Immunology Flashcards

1
Q

Hot T-bone stEAK

A

Hot T-bonestEAK = HoT BEAK

IL-1: fever (hot).

IL-2: stimulates Tcells.

IL-3: stimulates bonemarrow.

IL-4: stimulates IgE production.

IL-5: stimulates IgAproduction.

IL-6: stimulates aKute-phase protein production.

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2
Q

ain’t too proud 2 BEG 4 help

A

Interleukin 4 induces T-cell differentiation into Th (helper) 2 cells, promotes B-cell growth, enhances class switching to IgE and IgG

(ain’t too proud 2 BEG 4 help)

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3
Q

Clean upon aisle 8

A

“Clean upon aisle 8.” Neutrophils are recruited by IL-8 to clear infection

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4
Q

Th1 cells: immunity type, function, secretes, result

A
  • cell mediated (everything except bacteria)
  • activates macs and cytotoxic T cells
  • secretes IFN gamma, IL-2, lymphotoxin beta
  • result: delayed hypersensitivity, cytotoxicity
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5
Q

Th2 cells: immune type, function, secretes, results

A
  • humoral
  • activates B cells, promotes class switching
  • IL-4, 5, 10, 13
  • result: secretion of antibodies
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6
Q

IL-12 and IFN gamma do what to a Th0?

IL-4 stimulates Th0 to do what?

A
  • stimulates conversion to Th1 cell
  • stimulates conversation to Th2
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7
Q

Steps in inflammatory leukocyte accumulation (1-5)

A

Margination–> rolling (selectins) –> slow rolling (activation of integrins)–> Tight adhesion (Mac-1/LFA-1) + crawling (ICAM-1) –> transmigration (PECAM-1)

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8
Q

Leukocyte Adhesion Deficiency syndromes: type 1

A
  • recurrent skin infections without pus formation
  • delayed umbilical cord detachment
  • Results from CD18 deficiency –> deficiency of beta-2 integrins (Mac-1/LFA)
    • effects tight adhesion, crawling, and transmigration
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9
Q
A
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10
Q

Parasitic defense initiation

A

IL-5 secreted by Th2 and mast cells –> eosinophil proliferation and activation

parasite coated wtih IgG and IgE –> abs bind Fc receptors on eosinophil surface –> eosinophil release Major Basic Protein –> ROS

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11
Q

a parasite causes an eosinophil to release major basic protein. what kind of immune response is this?

A

antibody-mediated cell-mediated cytotoxicity

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12
Q

upper respiratory infection followed by…one week later

  • palpable purpura
  • arthalgias
  • abdominal pain
  • intussusceptions
  • hematuria
A

Henoch-Scholein purpura

IgA immune complex mediated vasculitus

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13
Q

Henoch-Schonlein purpura

A

IgA immune complex mediated vasculitis

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14
Q

TNF-alpha

A
  1. Activates endothelium.
  2. Causes WBC recruitment, vascular leak.
  3. Causes cachexia in malignancy.
  4. Maintains granulomas in TB.
  5. IL-1, IL-6, and TNF-α can mediate sepsis
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15
Q

Interleukin-2 and IL-3

stimulated by who and does what?

A

Interleukin-2

all cell types

Stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells.

Interleukin-3

all cell types

Supports growth and differentiation of bone marrow stem cells. Functions like GM-CSF

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16
Q

“acute then recruit” ilterleukins

A

acute (IL-1, IL-6, TNF-α), then recruit (IL-8, IL-12)

17
Q
  1. hyperacute transplant rejection–>
  2. acute transplant rejection –>
  3. chronic transplant rejection –>

CD markers for each?

A
  1. preformed antibodies (Typ II HSR): minutes to hours, gross mottlings and cyanosis, arterial fibrinoid necrosis and capillary thombotic occlusion
  2. CD8/CD4/Th2 activation: less than 6 months
    1. humoral: Cd4 deposition, neutrophilic infiltrate, necrotizing vasculitis
    2. cellular: lymphocytic, interstitial infiltrate, endotheliitis
  3. months to years–> vascular wall thickening, luminal narrowing, interstitial fibrosis and parenchymal atrophy

CD20 is a B cell marker. B cells are involved in hyperacute rejection as well as the humoral type of acute rejection.

CD27 is a marker of plasma cells. Plasma cells are involved in hyperacute rejection.

CD34 is a marker of fibrocytes, which are involved in chronic rejection.

CD4 and CD8 markers of helper T cells: acture rejection. Helper T cells are also involved in chronic rejection.

CD56 is a marker of natural killer cells. Natural killer cells are involved in hyperacute rejection.

18
Q

triad: thrombocytopenia, eczemia, combined T/B cell deficiency

A

Wiscott-Aldrich Syndrome

19
Q

ambulatory incoordination, spider angiomas, combined T/B cell deficiency

A

ataxia telangectasia

the A’s:

  • angiomas
  • ataxia
  • IgA deficiency
  • ATM gene
20
Q

deficient CD40L-CD 40R interactions

A

hyperimmunoglobin M syndrome

21
Q

Lung Transplant Rejection: hyperacute, acute, chronic

A

hyperacute: minutes to hours, preformed antibodies
acute: cell mediated response to mismatched donor HLA
chronic: cell mediated response to HLA, slow and progressive

22
Q

Reactive Arthritis:

  1. preceding genitourinary infection
  2. preceding enteritis
A
  1. GU infection: chlamydia trachomatis
  2. Enteritis: Salmonella, Shigella, Campy, Clostridium, Yersnia

tsomkapQ (117 decks)

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