When an individual is exposed to a specific antigen (aller-gen) that reacts with IgE antibodies bound to the surface of mast cells or basophils via their high-affinity receptors (FcεRI), it initiates mast cell activation. This type of IgE-dependent activation initiates a cascade of events, result-ing in allergic reactions. These reactions can occur as immediate hypersensitiviy reactions, (usually within sec-onds to minutes after exposure to an allegen), late-phase reactions, or chronic allergic inflammations. The immediate hypersensitivity reaction involves IgE-mediated release of histamine and other mediators from mast cells and also from basophils. The clinical symp-toms caused by the above mediators vary, depending on which organ system is affected. The release of mediators in the superficial layers of the skin can manifest as erythema (redness), swelling and itch-ing, or pain sensations. Respiratory system symptoms in-clude sneezing, rhinorrhea (runny nose), increased production of mucus, coughing, bronchospasm (constric-tion of bronchi), and pulmonary edema. Individuals with these symptoms often complain of tightness in the chest, shortness of breath, and wheezing. The gastrointestinal tract can also be affected with symptoms of nausea, vomit-ing, diarrhea, and abdominal cramping. In highly sensitive individuals, the antigen injected by an insect can trigger a massive discharge of mast cells and ba-sophil granules that affect more than one system. This con-dition is known as anaphylaxis. Dilation and increased permeability of systemic blood vessels can cause anaphy-lactic shock. This often-explosive, life-threatening reaction is characterized by significant hypotension (decreased blood pressure), decreased circulating blood volume (leaky vessels), and smooth muscle cells constriction in the bronchial tree. The individual has difficulty breathing and may exhibit a rash, as well as have nausea and vomiting. Symptoms of anaphylactic shock usually develop within 1 to 3 minutes, and immediate treatment with vasoconstric-tors such as epinephrine is required. The assessment of the activation of basophils in systemic anaphylactic reac-tions is still problematic because an assay for a specific cellular marker released by basophils (and not by other cells such as mast cells) has not yet been developed. After the signs or symptoms of the immediate hyper-sensitiviy reaction have been resolved, an affected indi-vidual may develop late-phase allergic reactions 6 to 24 hours later. The symptoms of these reactions may in-clude redness, persistent swelling of the skin, nasal dis-charge, sneezing, and coughing, usually accompanied by an elevated white blood cell count. These symptoms usu-ally last a few hours and then disappear within 1 to 2 days of the initial allergen exposure. In the respiratory system, the late-phase reaction is believed to be responsible for the development of persistent asthma. If the exposure to an allergen is persistent (for instance by a dog-owning patient who is allergic to dogs), it can result in chronic allergic infammation. Tissues in such individuals accumulate variety of immune cells, such as eosinophils and T lymphocytes that cause more tissue dam-age and prolong inflammation. This can lead to permanent structural and functional changes in the affected tissue.
bone marrow stromal cells (BMSCs) that can generate chondrocytes, osteoblasts, adipocytes, muscle cells, and endothelial cells. The MAPCs are adult counterparts of embryonic stem cells. Niches of adult stem cells called mesenchymal stem cells are found in loose connective tissue of the adult. These cells give rise to differentiated cells that function in the repair and formation of new tissue such as in wound healing and in the development of new blood vessels (neovascularization).
The vascular pericytes found around capillaries and venules are mesenchymal stem cells.