Page 966 - Veterinary Immunology, 10th Edition
P. 966

lung. They contain chondroitin sulfate but little histamine.
  VetBooks.ir  Connective tissue mast cells, in contrast, arise from fetal liver stem

               cells. They are found in the skin, around blood vessels, and in the
               peritoneal cavity. They are rich in histamine and heparin. Although

               connective tissue mast cell numbers remain relatively constant,
               mucosal mast cells proliferate in the presence of intestinal worms.
               Connective tissue mast cells are constitutive and T cell
               independent, while mucosal mast cells must be induced and are T

               cell-dependent. Induced mucosal mast cells disappear within a few
               weeks after the parasites are eliminated.



               TABLE 29.1
               Comparison of the Two Major Types of Mast Cell



                           Mucosal Mast Cells    Connective Tissue Mast Cells
                Structure  Few, variable-sized granules Many uniform granules
                Size       9 to 10 µm diameter   19 to 20 µm diameter
                Proteoglycan Chondroitin sulfate  Heparin
                Histamine  1.3 pg/cell           15 pg/cell
                Life span  <40 days              >6 months
                Location   Intestinal wall, lung  Peritoneal cavity, skin
                  Many different stimuli trigger mast cell degranulation. The best
               recognized of these are specific allergens linked to IgE. Allergies,

               however, are but a special type of inflammation. Numerous other
               signals can degranulate mast cells, including cytokines,
               chemokines, chemical agents, physical stimuli, insect and animal

               venoms, and viruses. Many DAMPs, including the defensins,
               anaphylatoxins, IL-33, neuropeptides, adenosine, and endothelins
               (small peptides from endothelial cells), also trigger mast cell
               degranulation.
                  Mast cells express multiple pattern-recognition receptors,

               complement receptors, and the mannose receptor (CD48).
               Triggering of their toll-like receptors (TLRs) causes mast cells to
               release different mixtures of mediators. Thus bacterial

               peptidoglycans acting through TLR2 stimulate histamine release,
               whereas lipopolysaccharides acting through TLR4 do not. Bacterial
               binding to mast cell TLRs triggers tumor necrosis factor-α (TNF-α)
               and IL-6 production. Mast cells can thus use these receptors to
               distinguish between different pathogens and release a select

               combination of cytokines, chemokines, and other inflammatory





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