Shigeo Yamagishi

Revisiting the roles of mast cells in allergic rhinitis and its relation to local IgE synthesis.

Mast cells are important effector cells in the immediate-phase allergic reaction. However, in recent years much evidence has accumulated on the versatile role of mast cells in allergic inflammation. The present article is an overview of the roles of mast cells in allergic inflammation, especially in light of the local production of IgE and the IgE-IgE receptor network. Although both nasal mast cells (NMC) and T cells in allergic rhinitics are important sources of Th2-type cytokines like IL-4 and IL-J3, and can induce IgE synthesis, we report here that antigen-activated NMC can secrete greater levels of IL-4/IL-13 and induce increased levels of IgE synthesis than antigen-activated nasal T cells. Furthermore, IgE production can occur locally in the nasal mucosa (target organ) and IgE itself can enhance the Fc∊RI expression and subsequent mediator release from NMC, thus contributing to the perpetuation of on-going allergic inflammation. Again, mast cells can contribute to the late-phase allergic reaction not only via the upregulation of adhesion molecules like VCAM-1, but also through the interactions of NMC with the extracellular matrix proteins, and interaction of NMC with nasal epithelial cells (NEC). Thus, it is increasingly evident that mast cells are not only important for the genesis of the allergic reaction, but also contribute to the late-phase allergic reaction and on-going allergic inflammation.

Mast cell-IgE-and mast cell-structural cell interactions in allergic airway disease.

Allergic diseases like atopic rhinitis, bronchial asthma, and urticaria are prevalent and on the rise. Mast cells are known to play a central role in the immediate phase reaction of allergic diseases through the IgE-mediated release of a variety of chemical mediators like histamine, leukotrienes, and prostaglandins. On the other hand, T lymphocytes, basophils and eosinophils are thought to be responsible in inducing the late phase response. Yet, recent studies show that the mast cell cannot be simplistically assigned a role in the immediate phase allergic response, and that this cell plays a crucial role in ongoing allergic inflammation, including the development of hyper-responsiveness. In the present article, the author will try to discuss the integrated roles of mast cells in IgE-mediated allergic inflammation with specific emphasis on the roles of mast cell-IgE networking and mast cell-structural cell interactions in the late phase allergic response and chronic allergic inflammation.

Increased expression of HLA‐DR and CD86 in nasal epithelial cells in allergic rhinitics: antigen presentation to T cells and up‐regulation by diesel exhaust particles

Background A proportion of nasal epithelial cells (NEC) in patients with allergic rhinitis (AR) are known to express the major histocompatibility complex Class II molecule (HLA‐DR).

Pathophysiologic mechanisms of chronic rhinosinusitis

Rhinosinusitis is one of the most common disorders and is a major health problem worldwide. This multifactorial disease has a complex nature, and the limited understanding of its relationship with associated factors makes it difficult to precisely define and classify. Broadly speaking, rhinosinusitis may be defined clinically as a condition manifested by an inflammatory response involving the mucous membranes of the nasal cavity and paranasal sinuses. Because of the heterogeneous nature of chronic rhinosinusitis, further studies are essential to a good understanding of the mechanisms that cause this pathology.

Novel Roles of Mast Cells in Modulating IgE-Mediated Allergic Inflammation

Mast cells play a central role in the immediate-phase allergic reaction through the IgE-mediated release of a variety of chemical mediators such as histamine, leukotrienes and prostaglandins. On the other hand, T lymphocytes, basophils and eosinophils are thought to be responsible for inducing the late-phase response. Yet, whether the mast cell can be simplistically assigned a role in the immediate-phase allergic reaction, and whether the cell is necessary for the ongoing allergic response, including the development of hyperresponsiveness, remain to be completely studied. Here, we will discuss the integrated roles of mast cells in IgE-mediated allergic inflammation.