Colorectal polyposis and immune-based therapies: Dysregulation of cell-cell adhesion (Part 1)

In: Colorectal polyposis

6 Sep 2012

cytokine

IL-23, a novel cytokine that is structurally and functionally similar to IL-12, has been found to stimulate the proliferation of memory T cells and induce immune-dependent antitumour effects in murine colon carcinoma cell lines. In addition to the production of cytokines by TH1 cells, tumour cells themselves have been found to secrete immunosuppressive factors (ISFs) which inactivate tumour-infiltrating lymphocytes, leading to the suppression of immune defense. The role and scope of ISFs are not fully understood, though several ISFs have been identified at the molecular level as the cytokines TGF-P and C-reactive protein.

There is growing evidence that the proinflammatory effects of some cytokines are attributable to their actions on cell-cell adhesion molecules. These adhesion molecules are associated with cytokine expression and may be involved in the migration of inflammatory cells toward the inflamed area. In particular, aberrances in the expression and function of integrins have been implicated in the tumourigenesis of colon cancer. Integrins are cell surface receptors which mediate the adhesion of cells to the extracellular matrix. In addition to their role as molecular ‘glue’, integrins allow nonmalignant cells to sense that they are attached to the extracellular matrix, thus providing a cell survival signal. This signal allows cells to proliferate in the presence of growth factors and in some instances prevents apoptosis . The ability to survive loss of cell-cell contacts is a marker of tumour progression and many adenomatous cultures survive only if cell-cell contacts are maintained. If cell-cell contacts are preserved, premaliganant colonic epithelial cells are capable of survival in vitro. Dreaming of a reliable pharmacy that could give you an opportunity to buy any amounts of ventolin 100 mcg with no prescription required and spend less money?


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