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Cell‐mediated immune responses in oral disease: A review
Author(s) -
Lehner T.
Publication year - 1972
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1972.tb02138.x
Subject(s) - immunology , immune system , antibody , oral mucosa , cytotoxic t cell , cellular immunity , lymphocyte , antibody dependent cell mediated cytotoxicity , biology , immunity , medicine , microbiology and biotechnology , pathology , biochemistry , monoclonal antibody , in vitro
. A review of cell‐mediated immunity in oral disease suggests that Gram‐negative bacteria, fungi, viruses and oral mucosa may give rise to 4 groups of immune responses. In gingival and periodontal disease (Group I), lymphocyte transformation is stimulated with dental plaque, Veillonella alcalescens, Fusobacterium fusiforme and Bacteroides melaninogenicus . Cytotoxicity against unrelated target cells and migration inhibition of macrophages also results from lymphocyte activation. The functions of lymphocytes are affected by serum factors which might prove to be antibodies or immune complexes. These data suggest that cell‐mediated immunity against a number of oral microorganisms may be involved in the pathogenesis of periodontal disease. Immunological studies in recurrent aphthous ulceration (Group II) suggest that oral epithelium or some antigenically cross‐reacting microorganism stimulates cell‐mediated and antibody responses. Autoimmune damage of oral mucosa, resulting in ulceration, can be accounted for by the immunological competence and cytotoxic potential of sensitized lymphocytes. Susceptibility to recurrent Herpes virus hominis type 1 infections (Group IIIA) may be accounted for by a selective and specific impairment of production of migration inhibitory factor and cytotoxicity in the presence of intact lymphocyte sensitization and antibody formation. Chronic muco‐cutaneous candidosis (Group IIIB) shows spectral immunodeficiencies with cell‐mediated and antibody defects which have been broadly related to the severity of clinical manifestations. Thus, in chronic oral hyperplastic candidosis the cellular immune defect may be limited to cytotoxicity, migration inhibition and sometimes impaired delayed hypersensitivity skin reaction to Candida albicans . Serum IgG and IgM antibodies are depressed also, but salivary IgA antibodies are raised and lymphocyte transformation is also intact. In the various histological stages of leukoplakia and in carcinoma (Group IV) there is a significant increase, mostly in lymphocytes and plasma cells. This is associated with a corresponding decrease in transformation of lymphocytes stimulated with autologous leukoplakic tissue. Cell‐mediated immune studies may show whether there is an impaired tumor surveillance in the leukoplakia‐carcinoma relationship.