title: B- and T-lymphocytes in ocular disease.
abstract: Ocular inflammatory diseases and ocular adnexal lymphoid tumors have become less obscure and intimidating by virtue of our ability to study the infiltrates in these various diseases for their B-lymphocyte and T-lymphocyte composition. Comparisons are also possible between lymphocytic profiles in the peripheral blood and the precise composition of the in situ infiltrates within the ocular tissue themselves. The availability of monoclonal antibodies, which can determine T-lymphocytic subsets such as T-helper cells and T-suppressor/cytotoxic cells, natural killer cells, and monocytes-histiocytes, has provided a powerful technology for the delineation of the distinctive immune composition of the inflammatory infiltrates, as well as any possible disturbances in T-cell immunoregulation. B-lymphocytes produce immunoglobulins, which may be misdirected as autoantibodies in local or systemic autoimmune diseases. Immunoglobulin-mediated and therefore B-cell derived conditions include vasculitis, progressive cicatricial ocular pemphigoid, Mooren's corneal ulcer, scleritis, and hay fever and vernal conjunctivitis. Other diseases in which B-lymphocytes, their immunoglobulin products or immune complexes formed with presently unknown antigens are potentially at fault are chronic non-specific uveitis; iridocyclitis in Behcet's syndrome; Fuch's heterochromic syndrome, ankylosing spondylitis, and Reiter's syndrome; Graves' disease; and idiopathic inflammatory orbital pseudotumor and myositis. T-cells do not produce immunoglobins, but rather secrete lymphokines or interact directly with receptors or determinants on viruses or target tissues (eg. immunosurveillance against neoplasia); it is possible that some autoimmune diseases are the result of neo-antigens on the surfaces of host tissues that have been coded for by a cryptic inciting virus. T-cell diseases include phlyctenulosis graft rejections, graft versus host disease, and possibly sympathetic ophthalmia and temporal arteritis. Natural killer cells are involved in many of the same diseases as cytotoxic T-cells, except that the former require no period of sensitization (natural immunity), whereas cytotoxic T-cells must undergo an antigen-specific blast transformation (acquired immunity of the delayed hypersensitivity type). In many diseases in which B-cell derived auto-antibodies are at fault, there may be local tissue or systemic T-cell imbalances, with a reduction in T-suppressor cells and a relative augmentation in T-helper cells, thereby facilitating production of misdirected auto-antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000911:Antibodies, Monoclonal / Q000032:analysis; D001327:Autoimmune Diseases / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D003231:Conjunctivitis / Q000276:immunology; D009877:Endophthalmitis / Q000276:immunology; D005128:Eye Diseases / Q000276:immunology*; D005134:Eye Neoplasms / Q000276:immunology; D006111:Graves Disease / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007105:Immune Complex Diseases / Q000276:immunology; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology; D007958:Leukocyte Count; D012397:Rosette Formation; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D007136:Immunoglobulins