Celiac disease in XXXX with @entity1723 : a condition with distinct changes in intestinal immunity?

@entity1 @entity11178 @entity778 @entity32190 @entity66 @entity1723 @entity403 @entity8265 @entity291
Two common chronic @entity66 ( @entity66 ) and @entity1723 ( @entity1723 )-result from complex pathological mechanisms where genetic susceptibility, environmental exposure, alterations in intestinal permeability and immune responses play central roles. In this study, we investigated whether these characteristics were universal for @entity66 independently of @entity1723 association. For this purpose, we studied 36 @entity1 with normal small-bowel mucosa and 26 @entity1 with active @entity66 , including 12 @entity1 with @entity1723 . In samples from the small-bowel mucosa, we detected the lowest expression of @entity11178 ( @entity11178 ) mRNA in @entity66 @entity1 with @entity1723 , indicating an increase in intestinal permeability. Furthermore, these samples displayed the highest expression of @entity403 ( @entity403 ) mRNA, a marker for regulatory T cells, as compared with other @entity1 groups. At the same time, serum levels of IgA antibodies specific for the @entity66 -related antigens deamidated gliadin and @entity8265 ( @entity8265 ) were the highest in @entity66 @entity1 with @entity1723 . In contrast, no significant differences were found in IgA or IgG antibodies specific for @entity291 beta-lactoglobulin or @entity32190 @entity32190 -derived proteins. There were also no differences in the transamidating activity of serum autoantibodies between @entity1 and control individuals. Our results show that @entity1 with @entity1723 and newly detected @entity66 exhibit severely altered intestinal permeability, strong local immune activation and increased immunoregulatory mechanisms in the small bowel. Further study is required to determine whether these extreme changes in this @entity66 subgroup are due to some specific environmental factors ( @entity778 ), unknown genetic effects or autoimmune reactions to antigenic targets in intracellular tight junctions.
