multifunctional purpose (don't have to go into too much detail -> more depth in following sections
pg700 Da silva et al
This is different to activation in that it's how the biogenesis of the mediators occurs, not how an antigen triggers the degranulation. pg 4 moon et al
706, de silva
<pubmed>25062998</pubmed> <pubmed>25452755</pubmed> <pubmed>12592295</pubmed>
<pubmed>22561833</pubmed> review on igE interactions: http://www.nature.com/nm/journal/v18/n5/full/nm.2755.html
<pubmed>21333342</pubmed> autophagy: http://www.sciencedirect.com/science/article/pii/S0091674910030381
Mast cells are sentinel cells that are found distributed within the connective tissue throughout the boy and play an important role in both acute and chronic inflammation. Mast cells that are coated with IgE antibodies specific for certain environmental antigens are triggered to release histamine and other cytokines that induce early vascular changes that are hallmarks of acute inflammation.
Role of mast cells in parathyroid bone disease
An increased number of mast cells in the bone marrow can be linked with parathyroid bone disease, most common of which being chronic hyperparathyroidism (HPT). Those suffering from HPT have a disturbed immune function, and mast cells play a major role in innate immunity. Parathyroid hormone (PTH) significantly increases the number of mast cells in those with HPT. There is a 5-fold increase in bone marrow mast cells in those with HPT as compared to the controls. Elevated levels of PTH increase migration of preoestoblastic fibroblasts to the bone surface, and while these generally differentiate into osteoblasts, the increased PTH levels cause terminal differentiation to be impaired. The accumulation of mast cells on bone surfaces as a response to elevated PTH levels lead to this PTH-induced peritrabcular fibrosis, and cause the excessive recruitment of fibroblasts on bone surfaces. An increase in kit- ligand expression causes the build up of mast cells, as it is a potent chemotactic factor for these mast cells. Combined with an increased PDFG-A gene expression, these peritrabcular mast cells promote fibrosis, ultimately leading to bone disease.