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Immunology > Autoimmune Disease 1 > Flashcards

Autoimmune Disease 1 Flashcards

1
Q

Diagnostic Criteria of Lupus

A
  • Need 4 out of 11: (4 SKIN RASH NIA)
    1. Malar Rash - butterfly rash over face, spare labia folds
    2. Photosensitivity
    3. Oral/Nasal Ulcers
    4. Discoid rash - looks like flesh eating and turns into scars - red raised, disc shaped
    5. Renal - glomerulonephritis - full house pattern of immunoflourescensce, protein or cellular casts in urine
    6. Arthritis - swelling in 2 or more joints without bone damage
    7. Serositis - inflammation of serous tissue lining lungs, heart, ab
    8. Hematologic cytopenias/hemolytic anemia
    9. Neurologic- psychosis or seizures
    10. Immunologic- anti DNA or Anti-Sm antibodies
    11. ANA - speckled
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2
Q

Autoantibodies of SLE

A
  1. dsDNA - high specificity for glomerulonephritis
  2. histone - drug induced lupus
  3. SSA/ Ro - highly associated with neonatal lupus
  4. SSB/ La
  5. Sm - high sensitivity for lupus
  6. RNP
  7. Anti0-ribosomal P
  8. Anti-phospholipid
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3
Q

Subsets of lupus

A
  1. discoid
  2. limited systemic - most common
    • ANA, arthritis, rash, ulcers
  3. Severe systemic -
    • renal and CNS symptoms
    • Anti-dsDNA involved in glomerulonephritis
  4. Hematologic
  5. Drug induced
  6. Anti-phospholipid antibody syndrom (APS)
  7. Neonatal - when the anti-ssa is transfered
    • can see the anti-Ro deposited btw dermal and epidermal layers
    • rash in the skin associated with neonatal lupus
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4
Q

Lab markers for SLE

A
  • Low complement levels (C3, C4) during flare ups
    • 90% are C1q deficient, 75% C4 deficient
  • elevated Sed Rate (ESR)
  • Eleveated dsDNA levels track disease activity
  • urnialysis - proteinuria and RBC casts
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5
Q

SLE pathophysiology (mechanism)

A
  • BLyS (BAFF) elevated
    • stimulates B-cell proliferation, survival
    • stimulates Ig Class switching
    • up in T-dependent immune responses
  • makes B-cells make more anti-self antibodies
  • also Type I IFNs genes are upregulated
    • more INF alpha which produced by TLR activation
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6
Q

treatment for lupus

A
  • corticosteroids
  • hydroxychloroquine - blocks MHC presentation to T-cells
  • Anti-BLys - targets B-cells
  • Anti-CD20/ rituximab - CD20 is on B-cells targets them
  • Anti-CD22 - epratuzumab - same thing
  • Anti-IFN- alpha
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7
Q

New Diagnostic Criteria for Primary Sjorgren’s Syndrome

A

2 out of 3 of the following criteria

  • Pos. SSA/Ro and/or SSB/La -OR- RF anddd ANA
  • Salivary gland biopsy >1
    • check for inflammation in small salivary glands -
    • look for accumulation of tertiery lymph organ - germinal centers and lymphocytes
  • severe dry eye with ocular staining - or Shirmer’s paper in eye test
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8
Q

Sjogren’s disease features glandular and extraglandular

A
  • Glandular
    1. Ocular - extreme dry eyes - shrimers test
    2. Oral - extreme dry mouth - needs liquids to swallow
  • Extraglandular
    1. Skin - cutaneous vasculitis, Raynauds
    2. Joints - arthritis, RF+, artralgias
    3. Lungs - interstitial ung disease
    4. Kienys - interstitial nephritis
    5. CNS - neuropathy
    6. General Fatigue
    7. muscles, hear, GI tract, hematologic
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9
Q

Diagnose Sjogren’s

A
  • Ocular signs - Schirmer’s test, Rose bengal staining
  • histopathology - lymphoid foci
  • Salivary gland involvement
    • ultrasound, salivary flow, radiographic or floursecent imaging
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10
Q

Sjogren’s treatments

A
  • Treat dry mouth with salivary replacements, meds to increase saliva
  • Dry eyes - artificial tears, cauterize eye drainage ducts, cyclosporin
  • Immunosuppressants
    • hydroxychloroquine - prevents antigen presentation MHC (glandular and arthritis)
    • Rituximab - binds the CD20 on B-cells - help with the oral and ocular dryness
    • methotrexate - arthritis
    • Azathioprine - helps ILD
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11
Q

Other diseases associated with Sjogren’s

A
  • Neonatal lupus (Anti-Ro/SSA)
  • lymphomas - ** big complication of sjogrens is lymphoma
  • Cavities, Thrust, Oral Candidiasis
    • decreased saliva not just about keeping mouth moist - lose the histatins and beta-defensins
    • IL-17 needed for activation of neutrophils and making these to resist oral candidiasis
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12
Q

Autoimmune Epithelitis - sjogren’s

A
  • trigger
  • epithelial cells attract T-cells - VCAM< MHC, B7, CD40 etc
    • attract B-cells CXCL13 chemokine
  • epithelial serve as APC and bring immune cells
  • BLyS activates B cells to form germinal centers and make antibodies
  • BAFF turns B-cells into plasma cells to make antibodies - overproudced by epithelial
    • Blys receptors highly expressed on transitional B-cells and required to develope - leads to overproduction of autoantibodies
    • salivary lymphoid foci
      • have lots of B-cells
      • tertiary lymphoid organs with gemr centers and transitional and marginal zone B cells
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13
Q

NOD2, ATG16L1

A
  • NOD2 - intracellular sensor of bacterial antigens in the gut
    • 30-40% of Crohn’s patients have a mutation at NOD2
  • ATG16L1
    • role in autphagy (lysosomes turnover of organelles)
    • ATG16L1 deificient Paneth cells (make anti-microbial in gut) are defective
  • NOD2 and ATG16L1 defects predispose IBD by perturbing the nroaml innate immune system to respond toward cmmensal flora required for the maintenance of tolerance
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14
Q

Two Drug targets in IBD

A
  • Natalizumab
    • prevents the interaction btw lymphocyte integrin Alpha4
      beta7 and MadCAM-1 adhesion molecule on endothelia cells
    • prevents the lymphocytes from going to site of
      inflammation
  • Infliximab - monoclonal antibody against TNF-alpha
    • prevents inflammation
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15
Q

Mechanisms of T-helper cells in IBD

A
  • Th1 cells produce INF-gamma and TNF-alpha leading to cellular immunity and inflammation
  • TH17 cells express IL-17 and IL-22 which increases mucosal immunity
  • Th2 - IL-4,5,13 increase humoral immunity
    • involved in the IL-23 axis and regulation of IBD susceptibility
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16
Q

Auto-antibodies of IBD

A
  • ASCA - 40-80% of Crohn’s (not usually UC)

- P-ANCA - 60-80% of UC

17
Q

Definition of Celiac’s

A
  • loss of immune tolerance to gliadin (antigen in wheat, barely, and rye)
  • mainly in small bowel after environemental trigger (infection)
  • loss of villi
  • aberrant innate immune response - propogated by a dysregulated adaptive immune response
18
Q

Celiac’s pathogenesis

A
  • infection - epithelial barrier breakdown allowing more gliadin to get to the lamina propria where APC cells are
    • Gliadin resistant to breaking down - so more to start
  • Genetic predisposition
    • individuals with G2/G8 MHC-II complexes have high affinity for Gliadin, efficient T-cell actvation in lamina propria
  • tissue transglutaminase makes gliadin even higher affinity
  • propagated by CD4, CD8, and intraepithelial gamma-delta T-cells
  • leads to lack of villi and malabsorption
19
Q

GPA triad

A

Granulomatosis with polyangiitis

  • vasculitis of upper and lower resp. tract
  • golmerulonephritis
  • necrotizing, granulomatous inflammation
20
Q

general progression of vascular inflammation

A
  • Neutrophils attracked - cause tissue damage in all layers of vessel wall
  • vessel normal response leads to more damage
    • aneurysms, narrowing, occlusions
21
Q

Common Clinical features

A

increased Sedrate, ANCA, RF+

  • Chronic sinusitis
  • nasal septal perforation
  • orbital pseudotumor
  • airway inflammation
  • subglottic stenosis
  • Renal complication - proteinuria, RBC casts - from the glomerulonephritis
  • purpura, petechiae
  • DVT
  • fatigure, chills, weight loss
22
Q

ANCA -

A
  • autoantibodies against neutrophils
  • C-ANCA + triad = 90% sensitivity
    • PR3 on neutrophils is what the antibody is against
  • ANCA activates the neutrophils
    • neutrophils express pro-inflam - TNF-alpha, IL-1, IL-8
    • increase adhesion and transmigration
    • antibody binding to pR3 on neutrophil - immune complex
  • PR3 induces DC cells to mature
  • DC migrate to LN and activate T cells, and promotes Th1 formation and granulomas
  • in vessels, ANCA antibodies promote more ahesion, transmigration, production of ROS, complement activation -> inflammation1
23
Q

Initiation of GPA

A
  • usually an infection upregulates B-cell and T-cells
  • primes neutrophils
  • ANCA
  • immune response to complement proteins - antibody production against them, then secondary antibodies

Immunology (20 decks)

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