The intestinal mucosa forms a primary barrier providing both barrier function and immediate effective recognition of bacterial products invading the mucosa. This is of great importance for the prevention of permanent and chronic inflammation as a reaction to the commensal intestinal flora and the multitude of antigens present in the intestinal lumen. It is obvious that a tight network of specialized cell types and intense cell-cell communication is required to maintain this function and coordinate immunological reactions. Yet most publications are focused on unidirectional cause and effectchains. Since a real integrated view on the network of cellular functions is not available or at least incomplete bidirectional immune cell interactions with epithelial cells, fibroblasts/myofibroblasts, adipocytes endothelial cells and the nervous system are reviewed in this article. Networking is certainly mediated by different effector pathways but limited resources are available to assemble a model of interactions in intestinal inflammatory diseases. However, recent development of knowledge regarding unidirectional and bidirectional effect-chains is exciting. Apart from the classical discrimination of immune cells (such as neutrophils, macrophages, and cytotoxic T cells) and non immune cells (epithelial cells, fibroblasts, adipocytes and endothelial cells) it became stunningly evident that not only the classical immune cells have the ability to track down pathogens as most of the mentioned cell types express pathogen recognition receptors (toll-like receptors, Nod2) and defense mechanisms (such as secretion of defensin).
Keywords: NK receptors, intestinal macrophages, adipose tissue, CD40L system, inflammation, nervous system
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