Patients with diabetes are at significant risk of developing corneal lesions, such as superficial punctuate keratitis, recurrent corneal erosions, persistent epithelial defects, and microbial keratitis. These lesions are all due to lacrimal gland dysfunction [1]. Even proliferative diabetic retinopathy appears to have a more severe course in patients with diabetes and declined tear film function [2]. Whether or not lacrimal gland dysfunction is metabolic or autoimmune in origin is still controversial [3]. Proliferative and non-proliferative retinopathies are metabolic complications of diabetes. These metabolic complications are caused by microangiopathy, the severity of which in turn determines the development of retinopathy as well as nephropathy and neuropathy. However, a causative relationship between metabolic complications of diabetes and non-retinal ocular disease (i.e., lacrimal dysfunction) is not well established. On the contrary, evidence exists for the association between "tear film" dysfunction (characteristic of diabetes-associated dry eye disease) and autoimmune diabetes [4]. Studies have recently established that the prevalence of symptoms, signs, and definitive diagnosis of dry eye syndrome (DES) are higher, and basal tear secretion and tear film stability are lower, in children with autoimmune (type 1) diabetes mellitus (T1D), years before metabolic complications are even expected [4]. Animal models of autoimmune diabetes have provided the strongest evidence for a causative relationship between autoimmunity and diabetes-associated DES. Non-obese diabetic (NOD) mice, the classic model of human T1D, usually develop lacrimal gland dysfunction. Autoimmune lymphocytic infiltration of lacrimal glands accompanies lymphocytic infiltration of pancreatic islets in NOD mice [5]. A possible explanation for this association of pancreatic islets and lacrimal gland lymphocytic attacks has been based on the existence of cross-reactive antigens in both glands. Recently, a special group of CD4+ helper T cells was observed to be enriched in the inflamed pancreas and salivary glands of NOD mice as well as in the circulation of Sjögren's syndrome patients [6].
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