Alterations in serum immunoglobulin G subclasses in patients with ulcerative colitis and Crohn's disease

Serum Immunoglobulin G Subclasses in Patients with Ulcerative Colitis and Crohn's Disease of Different Disease Activities

“…Our study, based on a large number of patients with different disease activities, confirms previous findings that plasma concentrations of the IgG subclasses IgGl and IgG2 differ in ulcerative colitis and Crohn's disease (2). These findings lend support to the theory that ulcerative colitis has immunologic characteristics consistent with an autoimmune disorder (increased IgG 1) (2).…”

“…These findings lend support to the theory that ulcerative colitis has immunologic characteristics consistent with an autoimmune disorder (increased IgG 1) (2). whereas Crohn's disease has immunologic characteristics consistent with a response to an infectious agent or stimulatory agents (increased IgG2).…”

Immunopathogenesis of chronic inflammatory bowel disease

“…Histopathological studies also revealed that the initial lesion in ulcerative colitis is on the epithelium, and that the inflammatory response seems to be secondary. Increased serum levels of autoantibodies to colonic epithelium and epithelial deposition of immunoglobulins within deposits of complement activation products, apically on the colonic epithelium of patients with active ulcerative colitis, suggest that ulcerative colitis may be caused by an IgG-mediated autoimmune process to colon mucosa (28)(29)(30).…”

“…Conversely, IgG2 levels seemed to be increased in Crohn's disease, whilst they were normal in ulcerative colitis. IgG3 and IgG4 levels were not altered in chronic inflammatory bowel disease (29).…”

Ulcerative colitis in a renal transplant patient with previous Goodpasture disease

“…Environmental factors such as antibiotics, non-steroidal anti-inflammatory drugs, and respiratory infections may be triggers for the disease [4][5][6]. Defects in immunoregulation include abnormalities in epithelial antigen presentation, increased macrophage activity, decreased IL-1 inhibition, increased secretion of the TH2 lymphocyte cytokines, IL-4 and IL-10, and increased IgG1 production [7][8][9]. The theoretical link between the pathogenesis of ulcerative colitis and anti-GBM disease is a failure to recognize self.…”