Background: Chronic progressive conjunctival cicatrization is found in some mucocutaneous disorders (cicatricial pemphigoid, linear IgA disease) and after long-term treatment with certain topical medications (pseudo-pemphigoid). Little is known about the mechanisms of conjunctival shrinkage, and therapy for these conditions remains difficult.
Objectives: To elucidate the immune mechanisms and assess the main factors involved in conjunctival scar tissue formation in patients with chronic progressive conjunctival cicatrization.
Patients and method: We examined 14 bulbar conjunctival biopsy specimens from patients with chronic progressive conjunctival cicatrization (8 with benign mucous membrane pemphigoid confirmed by biopsy, 4 with the ocular features of benign mucous membrane pemphigoid and 2 with pseudopemphigoid) and 10 biopsies from matched healthy individuals: 1.5 mm sections of glycol methacrylate embedded tissue were analysed with the aid of a panel of monoclonal antibodies.
Main results: Cell counts in the subepithelial substantia propria showed a marked increase in T-cells over normal controls (up to 30-fold). Among the T-cell subsets, there were more CD8 than CD4-positive cells observed. Only about 5% of the T-cells were activated (IL-2 receptor-positive). Macrophages were--as in normal tissues--the second most predominant cell. The absolute number was 2-3 times as high in diseased conjunctiva as in controls. There was increased expression of MHC II molecules on macrophages, lymphocytes und fibroblasts. The numbers of B-cells and NK were not increased.
Conclusions: The analysis of the cellular infiltrate showed nonspecific immunopathological characteristics. Thus, the cellular infiltrate gives no explanation for the progressive cicatrization. There is evidence that soluble factors, especially fibrogenic cytokines, play an important role.