Eosinophil-Lymphocyte Interactions

A large number of cells are involved in the immune response and all are derived fiom the multipotential stem cells of the bone marrow. The predominant cell is the lymphocyte but monocytes-macrophages, endothelial cells, eosinophils and mast cells are also involved with certain immune responses. The two types of immunity (humoral and cell-mediated) are dependent on two distinct populations of lymphocytes, the B cells and the T cells respectively. Both the humoral and the cell-mediated systems interact to achieve an effective immune response. 

The development of respiratory hypersensitivity requires an induction phase where exposures to the sensitizer lead to an interaction with immune cells and the eventual development of specific effecter immune molecules (e.g., antibodies) and cells (e.g., T lymphocytes) [5], The induction phase can require months to years of exposure before there is a detectable immune response and/or onset of symptoms typical of respiratory hypersensitivity, including asthma. Classic IgE mediated responses have been described as Th2 cell dominant responses. A subset of CD4+ T cells known as Th2 cells push the immune response to the development of IgE and IgG4 antibodies in humans along with secretion of cytokines that attract and activate inflammatory cells such as eosinophils. 

Nakayama, H., Sano, H., Nishimura, T., Yoshidi, S., and Iwamoto, I. (1994) Role of vascular cell adhesion molecule 1/very late activation antigen 4 and intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 interactions in antigen-induced eosinophil and T cell recruitment into the tissue. J. Exp. Med. 179,1145-1154. 

The predominance of inflammatory changes in the fascia suggests that mediators produced by mesenchymal cells (fibroblasts and endothelial cells) may also play a role in the pathogenesis. For example, fibroblasts augment IL-5-dependent eosinophil survival and stimulate conversion to the hypodense phenotype. Fibroblasts can also produce IL-8, which recruits neutrophils and lymphocytes when injected in vivo. Thus, one can speculate that the etiologic agent interacts with these cells to stimulate release of inflammatory mediators and increase collagen synthesis. 

Although absent from the surface of resting endothelial cells in culture the expression of VCAM-1 is induced by IL-1, IL-4, and TNF-a but not IFN-y.44-46 Endothelial VCAM-1 supports the adhesion of lymphocytes and monocytes (but not neutrophils) through interaction with VLA-4,45 47 and this recognition mechanism could lead to the accumulation of mononuclear cells during the transition from acute to chronic inflammation. It appears that VCAM-1 also underlies eosinophil and basophil adhesion to activated endothelium.48... 

The present volume summarizes the state of information on chemokines focussing on skin diseases. The first three chapters deal with the structure and molecular biology of chemokines and their receptors. The following three review information on the interaction of chemokines with lymphocytes, mast cells and eosinophilic granulocytes. One chapter deals with the expression of chemokines in several inflammatory skin diseases. The final chapter reports on in vitro evidence for a growth-promoting activity of chemokines in skin-derived tumor cells. 

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