steele Flashcards

1
Q

describe the length of time of the mucosal immune response

A

FAR SHORTER

  • mucosal antibody responses = months to a year
  • serum antibodys = persist for decades
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2
Q

physical mechanisms of defense in GI tract

A
  • High acidity of stomach –> retards bacterial growth
  • Peristaltic motility, detergent action of bile, secretion of mucus limits uncontrolled growth
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3
Q

Gut-associated lymphoid tissue (GALT)

A
  • GALT = mucosal inductive sites
    • peyer’s patches, appendix, lymphoid aggregates in appendix and large intestine, lymphoid cells in lamina propria
      • Peyers patch = important in promoting IgA production and CTL response
  • Most GALT sites have distinct B cell follicles and T cell areas, with antigen presenting cells present
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4
Q

Peyer’s patches

A
  • Dome epithelium = M-cells with cell membrane microfolds
    • M cells transfer antigens from gut lumen to lymphoid tissue
      • PRESENT by APC’s to T helper cells
  • T cell rich parafollicular areas and distinct B cell rich follicle
  • Endocytosis or phagocytosis used to take up antigens from gut:
    • M cells interact physically with underlying APC’s and activate T cells
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5
Q

Intraepithelial lymphocytes (IEL)

A
  • epithelial cells of the GI tract for the intestinal lumen:
    • IEL;s are composed PRIMARILY of T LYMPHOCYTES
    • lymphocytes are in epithelium –> exposed to mucosal antigens
    • CN8+ IEL possess cytotoxic function –> cell-mediated immunity against viral + intracellular bacterial infections
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6
Q

Immune system cells of the lamina propria

A
  • cells in lamina propria composed mianly of CD4+ t cells
    • vast numbers of B lymphocytes, plasma cells, macrophages, dendritic cells, eosinophils and mast cell
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7
Q

Role of IgA

A
  • major immunoglobulin in secretions (saliva, mcuus, sweat etc)
  • Prevents binding of microbes to epithelila and facilitates expulsion
    • opsonizes small pathogens for pahgocytosis
    • eosinophil degranualtion via the FcalphaR for anti-parasite immunity
  • IgA from lamina propria can diffuse into extracellular tissue spaces, drain into lymphatic system and transported into blood stream
    • from bloodstream –> excreted into the gut via the bile
    • OBSTRUCTIvE JAUNDICE (don’t excrete bile) = Increase plasma IgA
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8
Q

Immune response in the GI tract

A
  1. M cells take up antigen by endocytosis and phagocytosis
  2. antigen is transported accross teh M cell in vesicles and released at basal surface
  3. antigen is bound by dendritic cells, which activate T cells
  4. T cells enter Peyer’s patches from blood vessels and encounter antigen transported across M cell and become activated by dendritic cells
  5. Activated T cells drain via mesenteric lymph nodes to thoracic duct and return to the gut via bloodstream
  6. activated T cells target the lamina propria and intestinal epithelilium of the small intestine
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9
Q

role of pre-plasma cells

A

Pre-plasma cells –> form plasma cells and secrete IgA

  • IgA binds to poly-immunoglobulin receptors –> transported across the cell and delivered onto the mucosal surface
  • IgA antibodies bind to microbes, preventing access to epithelium + promoting clearance
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10
Q

Mast cells

A
  • beneath epithelia exposed to environement
  • normal immunity = IgE-mediated defense against parasties
  • eliciting food-induced allergic reactions
    • diarrhea, anaphylactic shock
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11
Q

Oral tolerance

A
  • immunization with antigen via the GI tract can induce systemic unresponsiveness
    • prevents hypersensitivity reactions to ingested food proteins
  • Dose of oral antigen
    • High Dose –> clonal deletion of antigen-specific lymphocytes
    • Low Dose –> clonal anergy (unresponsiveness) + regulatory T cells suppress immune responses
      • regulatory T cells developed in GALT can migrate systemically
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12
Q

SELECTIVE IgA deficeincy

A
  • not typically assocaited with clinical problems SINCE mucosal transport of IgM can compensate for absence of IgA
  • Assocaited iwth greater risk for autoimmune disorders
    • due to absorption of intestinal macromolecules that mimi self antigens –> may stimulate autoimmune responses
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13
Q

Food hypersensitivites

A
  • Some reactions to food proteins are the result of IgE-mediated immediate hypersensitivity rxns:
    • nausea, vomiting, abdominal pain, and skin rashes
    • pharyngeal edema and bronchospasm may be seen
    • some food hypersensitivites –> fatal anaphylactic rxns
    • vasoactive amines (principally histamine) –> severe changes in vascular permeability –> massice protein-losing enteropathy and hypoalbuminemia
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14
Q

Gluten-sensitive enteropathy

A
  • Disease of SMALL INTESTINE –> malabsorption due to villous atrophy:
    • celiac sprue and idiopathic sprue
    • hypersensitivity to gliadin (family of proteins in wheat gluten)
    • epithelial cell lining intact, but functions abnormally
    • confined to small intestine -_> gliadin not broken down into a.a.
  • B and T cell infiltrates present in the lesion
    • anti-gliadin IgA may play role in pathogenesis, main mediator of damage appears to be T cells
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15
Q

Ulcerative colitis

A
  • Relatively superficial inflammation limited to the large bowel:
    • Ulcer formation and loss of mucosal absorptive function
  • If anti-inflammatory or immunosuppressive therapy not sufficient to control disease –> total colectomy:
    • surgery definitive since disease doesn’t affect small intestine
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16
Q

Crohn’s disease

A
  • Inflammatory + Granulomatous lesions commonly involving terminal ileum and ascending colon:
    • obstructive sympomes abscess formation and fistulas leading from bowel to other organs
    • failure of inflammatory macrophages to die by normal apoptotic mech following a response to normal gut flora
  • TNF-alpha –> plays role in disease rpocess
    • INFiXIMAB = reduces signs/symptoms of disease
17
Q

Pernicious anemia

A
  • Deficiency of vit B12 –> megaloblastic anemia + neuropathy
  • Most common cause = autoimmune antibodies against intrinisc factor (binds B12) or gastric parietal cells (produce intrinsic factor)
    • anti-instrinsic factor antibodies prevents vitamin B12 binding
    • RESULT = Vit B12 can’t be transported itno circulation