ABSTRACT
Celiac disease (CD), with a 1 percent worldwide prevalence, is an enteropathy caused by an autoimmune reaction to gluten in genetically susceptible individuals, which codify for histocompatibility molecules HLA DQ-2/DQ-8. From the anatomical point of view, CD is characterized by intestinal villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis (IELs) and leukocyte infiltration of the lamina propriety. Patients achieve a complete clinical and endoscopic remission with a gluten free diet. However, symptoms and anatomical alterations recur when this protein is reintroduced in the diet. The pathogenic mechanisms in this disease are not yet well understood, but it is clear that genetic, environmental and immunological factors play a role. The latter are the focus of this review, since this is the only autoimmune disease whose precipitating factor for immunological tissue damage is known.
Subject(s)
Humans , Celiac Disease/etiology , Diet, Gluten-Free , Intestinal Mucosa/immunology , Celiac Disease/pathology , Gliadin/immunology , HLA-D Antigens/immunology , Intestinal Mucosa/pathologyABSTRACT
Objective To investigate the expression of Human leucocyte antigen(HLA)-DP,-DQ,-DR and CD40 in human retinal pigment epithelial(RPE)cells,to determine their molecule expression in immune response process,and their abilities to stimulate T lymphocyte activation. Methods Human RPE cells were cultured with or without(-IFN respectively.Expression of HLA-DP,-DQ,-DR and CD40 was measured by immunohistochemical staining.Meanwhile,peripheral blood mononuelear cells(PBMC)were co-cultured with RPE cells in vitro,and then the expression of activated lymphocytes CD69 was measured by fluorescence activated eell sorter(FACS). Results Expression of HLA-DP,-DQ,-DR and CD40 antigen were enhanced by γ-interferon inducement.Increasing amount of CD69 positive Iymphocytes were found in the co-culture system of RPE cells and PBMC. Conclusion T-lymphocytes in the peripheral blood were activated by human RPE cells which is antigen presenting cells with immunological characteristics potential.
ABSTRACT
Objective To investigate the feasibility of using anti-sense RNA against classⅡmajor histocompatibility complex(MHCⅡ)transactivator(CⅡTA),which might regulate MHCⅡexpression,to suppress the relative immune response.Methods Stable transfectants of dermal fibroblasts with pDarⅡ(pDarⅡ-D)were tested for the expression of classic MHCⅡ(HLA-DR,-DP,-DQ)antigens induced with recombinant human interferon-gamma(IFN-?).mRNA abundance of CⅡTA,and classic MHCⅡwas mea-sured by RT-PCR.IL-2mRNA expressed in T cells,stimulated by transfected dermal fibroblasts,was de-termined by mixed lymphocyte reaction.Results When induced with IFN-?,the expression of HLA-DR and-DP antigens on pDarⅡ-D was reduced by95.63%and87.89%,respectively.Meanwhile,the mRNA contents of CⅡTA and classic MHCⅡwere decreased significantly(P