Canine idiopathic keratoconjunctivitis sicca (iKCS) is considered an immune-mediated condition with lymphocytic infiltration of the lacrimal gland (LG) and nictitans gland (NG) leading to reduction in tear production. A recent report documented changes in T lymphocytes in LG of dogs after cyclosporine treatment for KCS but without giving data on the phenotype of the initial cellular infiltrate. The present study aims to describe the lymphocytic infiltrate in the NG of dogs with idiopathic KCS, with neurological KCS and of normal dogs.

Biopsies of NG were obtained from six dogs with idiopathic, presumed immune-mediated, KCS (iKCS) and 2 dogs with neurological KCS (nKCS) at the time of parotid duct transposition. NG from nine normal dogs euthanased for non-ocular and non-immunological disease were obtained at post-mortem. Tissues were fixed for 24 hours in buffered formol saline and then processed to wax embedding. Indirect immunoperoxidase histochemistry was performed using monoclonal antibodies directed against canine CD3 (T lymphocytes) and CD79a (B lymphocytes). Ten x40 fields were examined for each gland and numbers of labelled and non-labelled cells recorded blind with the person counting the cell populations unaware of the diagnosis given.

CD3+ T lymphocytes comprised 5.8±2.6% of cells within the NG in normal dogs. In NG from dogs with neurogenic KCS the percentage of T cells was 7.7±0.5% and in idiopathic KCS 14.3±4.1%, significantly raised at p=0.001. The mean percentage of CD79a+ cells in normal dogs was 1.1±5.9%, in dogs with neurogenic KCS 15±1.7% and in idiopathic KCS 18.2±8.5%, again significantly raised at p=0.038.

This study demonstrates that a predominantly T cell population is present in dogs with idiopathic KCS as is the case in human Sjogren's syndrome and mouse models of immune-mediated KCS. T cells were not, however, elevated in number in dogs with neurogenic KCS. B cells were raised in number in dogs with idiopathic KCS compared to those in normal dogs but interestingly also raised in dogs with neurogenic KCS, although not statistically significantly so given the small number of cases evaluated. The lack of elevated T cell numbers in neurogenic KCS suggests that the increased number in idiopathic KCS is a feature of the immunological cause of the disease and not merely an effect of tear deficiency. Increased T cell numbers suggest that iKCS is indeed an immunological and probably autoimmune disease; research further to evaluate lymphocyte population in the disease is necessary.