Ocular Mucosal Immunity

Mucosal immunity defends the ocular surface against antigenic challenge and microbial invasion. The principal effector site is the lacrimal gland, where immunoglobulin A (IgA) antibodies are produced. Nasal-associated lymphoid tissue and posterior cervical lymph nodes function as major inductive sites for tear IgA responses. Neural connections and systemic hormones maintain the integrity and function of the ocular surface. Neuroenzyme activities in the lacrimal gland are influenced by ocular infections, leading to reduced expression of acetylcholine and modulation of receptors on acinar cells and on plasma cells, thereby decreasing fluid and immunoglobulin secretion. T lymphocyte-dependent responses result in production of interleukin-4 in lacrimal glands, thereby influencing cholinergic enzyme activity affecting immune processes and lacrimal physiology. Furthermore, neuropeptides released into lymphoid structures or inflamed tissues are chemotactic for antigen-presenting cells and affect their interactions with T cells. Thus, in developing therapeutic approaches for treating dry-eye conditions and vaccination strategies to elicit protective ocular mucosal immune responses, the entire lacrimal functional unit should be considered.