Abstract
Epithelial cells, fibroblasts and smooth muscle cells together form and give structure to the airway wall. These three tissue forming cell types are structure giving elements and participate in the immune response to inhaled particles including allergens and dust. All three cell types actively contribute to the pathogenesis of chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD). Tissue forming cells respond directly to allergens through activated immunoglobulins which then bind to their corresponding cell surface receptors. It was only recently reported that allergens and particles traffic through epithelial cells without modification and bind to the immunoglobulin receptors on the surface of sub-epithelial mesenchymal cells. In consequence, these cells secrete pro-inflammatory cytokines, thereby extending the local inflammation. Furthermore, activation of the immunoglobulin receptors can induce proliferation and tissue remodeling of the tissue forming cells. New studies using anti-IgE antibody therapy indicate that the inhibition of immunoglobulins reduces the response of tissue forming cells. The unmeasured questions are: (i) why do tissue forming cells express immunoglobulin receptors and (ii) do tissue forming cells process immunoglobulin receptor bound particles? The focus of this review is to provide an overview of the expression and function of various immunoglobulin receptors.
Highlights
The most prominent chronic inflammatory diseases of the lung are asthma and chronic obstructive pulmonary disease (COPD)
The fact that remodeling of the airways persists after the environmental stimulus is gone, while inflammation depends on the presence of a stimulus, points out that the immune response may not always be the initiating factor for chronic inflammatory lung diseases [29, 30]
In the past two decades we accumulated knowledge of the immune response in chronic inflammatory lung diseases, but this knowledge did not help us to explain the entire pathology of asthma or COPD or of any other chronic inflammatory lung disease
Summary
The most prominent chronic inflammatory diseases of the lung are asthma and chronic obstructive pulmonary disease (COPD). COPD is characterized by chronic inflammation of the small airways, with similar pathologies known for asthma [10,11,12] These include airway constriction, hyperplasia, and hypertrophy of mesenchymal cells, increased mucus production, tissue remodeling, and tissue degradation, emphysema [10, 11]. The fact that remodeling of the airways persists after the environmental stimulus is gone, while inflammation depends on the presence of a stimulus, points out that the immune response may not always be the initiating factor for chronic inflammatory lung diseases [29, 30]. The current hypothesis is that chronic inflammatory lung diseases are causatively linked to an overreactive or out of control immune response to environmental factors [30, 31]. In the past two decades we accumulated knowledge of the immune response in chronic inflammatory lung diseases, but this knowledge did not help us to explain the entire pathology of asthma or COPD or of any other chronic inflammatory lung disease
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