Driss Zoukhri

TL;DR: The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease, finding the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation to be important.

TL;DR: The mechanisms leading to lacrimal gland dysfunction are still poorly understood, and Apoptosis, production of autoantibodies, hormonal imbalance, alterations in signaling molecules, neural dysfunction, and increased levels of proinflammatory cytokines have been proposed as possible mediators of lacrima gland insufficiency in disease states.

TL;DR: Elevated levels of IL-1beta, as they occur in Sjögren syndrome exocrine glands, may impair the secretory function of these tissues, and proinflammatory cytokines inhibit neurally mediated lacrimal gland secretion.

TL;DR: The results show that activation of nerves of lacrimal and salivary glands infiltrated with lymphocytes does not increase the release of neurotransmitters, which results in impaired secretion from these glands.

TL;DR: Cholinergic agonists, through M2 and/or M3 muscarinic receptors, and VIP, through VIPR2, regulate conjunctival goblet cell secretion, suggesting that gobleT cell secretion in vivo is under the control of parasympathetic nerves.