title: Immunology of trachomatous conjunctivitis.
abstract: Trachoma, a chronic follicular conjunctivitis caused by infection with Chlamydia trachomatis, is a leading cause of preventable blindness. The blinding complications are associated with progressive conjunctival scarring. Our immunohistochemical studies of conjunctival biopsies from children with active trachoma demonstrated the presence of both humoral and cell-mediated immune responses. Antichlamydial antibodies can neutralize Chlamydiae, block attachment and internalization of the organism, and can produce partial immunity. Our observations suggest a role for T-lymphocytes and cell mediated immunity in the genesis of conjunctival scarring. Conjunctival epithelial cells expressed major histocompatibility complex (MHC) class II antigens which might allow conjunctival epithelial cells to present Chlamydial antigens to T-cells enhancing the immune response. The epithelial cells expressing MHC class II antigens might present autoantigens to T-cells leading to induction of an autoimmune reaction. We have demonstrated that the conjunctival epithelial cells from patients with trachoma expressed interleukin (IL)-1 alpha and IL-1 beta. In addition, we have detected cytoplasmic expression of IL-1 alpha, IL-1 beta, tumor necrosis factor alpha and platelet-derived growth factor by macrophages. These cytokines have the potential to influence the remodeling and fibrosis observed in trachoma. Alterations of extracellular matrix components and collagen metabolism occur in the conjunctival tissue from patients with trachoma. New collagen type V formation was noted in active trachoma and scarred trachoma. The conjunctival tissue from patients with active trachoma contained increased amounts of collagen types I, III and IV. Scarred trachoma is characterized by marked increase in basement membrane--collagen IV and marked decrease in collagen types I and III. In addition, we demonstrated increased activity of gelatinase B and numbers of inflammatory cells containing gelatinase B in trachoma patients suggesting that this enzyme might be involved in matrix degradation and promotion of conjunctival scarring in trachoma.
authors.affiliation: Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia. abuasrar@KSU.edu.sa
authors.forename: A M
authors.initials: AM
authors.lastname: Abu el-Asrar
authors.forename: K
authors.initials: K
authors.lastname: Geboes
authors.forename: L
authors.initials: L
authors.lastname: Missotten
mesh_terms: D000818:Animals; D000917:Antibody Formation; D000942:Antigens, Bacterial / Q000032:analysis; D001706:Biopsy; D002648:Child; D003094:Collagen / Q000145:classification; D003228:Conjunctiva / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005802:Genes, MHC Class II / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D010641:Phenotype; D014141:Trachoma / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines; D003094:Collagen; D020780:Matrix Metalloproteinase 9