Immunological factors affecting the development of IBD
Over the past decade science has been able to identify the role that both immune and nonimmune systems play in the mediation of IBD. In this section we highlight the role of humoral immunity, Cell mediated immunity, nonimmune cells, mediators of immune regulation and inflammation, mediators of healing and injury, and Mediators of cell contact play in the development of IBD. Although dysfunctions in the immune system are not primary causes of IDB they play an integral part in the pathogenesis of IBD
- Mucosal B cells
The development o f IDB results in the production of a humoral response, marked by striking increases in the production of immunoglobulin G(IgG). These surges in IgG production can be used to distinguish between the two forms of IBD. Different subclasses of IgG are expressed in each of the two forms of IBD. Individuals affected by UC experience an increase in IgG1. Conversely, those affected by CD experience an increase in IgG2. - Autoantibodies and Autoantigens
Individuals Patients with IBD display an array of circulating antibodies that seldom correlate with disease activity. Anticolon antibodies are not disease specific, nor are they tissue specific. Despite the lack of specificity in most cases it has been found that serum antibodies to Saccharomyces cerevisiae (Baker's yeast) increase in individuals with CD but not in individuals with UC. - Antineutrophil cytoplasmic antibodies
Studies have found a high prevalence of perinuclear antineutrophil cytoplasmic antibodies (pANCAs) in individuals with UC. These antibodies are found in a lesser degree in individuals with CD. - Systemic Immunity
A study by Broberger and Perlmann indentified that immune cells (cytotoxic cells) implicated in the development of UC were capable of recognizing and destroying intestinal cells. - Mucosal T cells
CD can develop as a result of diffuse infiltration of the intestines by immune cells in the absence of obvious inflammation. CD68+ macrophages and lymphocyte cells can go by undetected in the "unaffected" mucosa of Individuals with CD and accumulate, resulting in tissue destruction and inflammation. - Monocytes and Macrophages
Macrophages have been found to be present in early IBD lesions, as illustrated by the presence of HLA- DR+ and ICAM-1+ cells in aphthous ulcers. - PMNs, eosinophils Basophils and Mast Cells
PMNs play a role in the amplification of inflammation in damaged tissues. Activation of mast cells leads to degranulation in IDB. - Epithelial cells
Individuals with IBD often express abnormalities in epithelial cell phenotype and function. An abnormality in epithelial cells in the colon results in the defective capacity to induce suppressor T cells. Over time this abnormality may lead to the amplification of local immune reactivity and inflammation. - Mesenchymal cells
Mesenchymal cells function as structural cells, producing a variety of extracellular matrix proteins, needed in intestinal fibroblasts. Alterations in the production of Mesencheymal cells leads to an increase in the production of collagen type III, resulting in a thickening of the intestinal walls of individuals with CD. - Nerve cells
There enteric nervous system connects the neuroendocrine system to the immune system in the gut. Alterations in enteric neuromuscular function affect both motility and inflammation. An increase in stress, increases enteric neuromuscular activity resulting in inflammation of the intestines. Inflammation of the intestines leads to an expression of different concentrations and receptor density for substance P in CD. This expression differs from that expressed in the UC involved mucosa. - Endothelial cells
Microvascular endothelial cells function as the " gate keepers "of inflammation. Damage to these cells, as in the case of IBD, enhance intestinal mucosal endothelial cells' capacity to bind leukocytes, resulting in the persistence of the inflammatory response. - Immunoregulator cytokines
Individuals affected by UC exhibit decreased Interleukin - 2 bioactivity in the intestinal mononuclear cells. This is not the case concerning individuals affected by Crohn's disease. Individuals with active CD exhibit an increase in IL-2 mRNA. The production of interferon gamma by the intestinal mucosal mononuclear cells has been thought to suppressed in both forms of IBD. However, spontaneous release of interferon gamma intestinal mucosal mononuclear cells increases interferon gamma mRNA expression by lamina propria mononuclear cells and the presence of interferon gamma secreting cells in actively inflamed mucosa. Research has found decreases in interleukin-4 in both individuals with UC and CD. Studies have found increases in interleukin 5 production in individuals with UC. A decrease in the production of interleukin 5 was found in individuals with CD. - Proinflammatory cytokines
Proinflammatory cytokines have been found in high concentrations in both Ulcerative Colitis and CD. Although not specific to IBD, high concentrations of IL-1 have been found in the gut. Elevated levels of Tumor necrosis factor - alpha have be associated with the development of UC and CD in children. IL-6 Levels have been found to be high in individuals with CD but not those with UC.
One of the most important developments in intestinal immunity is the realization that local immune cells are functionally integrated with nonimmune origin
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