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Cell‐mediated and humoral immunity against oral streptococci, neisseria, staphylococci, and adult human oral mucosa antigens in recurrent aphthous stomatitis
Author(s) -
DONATSKY O.
Publication year - 1978
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.1978.tb00604.x
Subject(s) - exacerbation , immunology , neisseria , antigen , microbiology and biotechnology , medicine , antibody , streptococcus , stomatitis , biology , bacteria , genetics
— Cell‐mediated immunity (CMI) and humoral immunity (HI) against oral bacteria ( Streptococcus sanguis strain 2A, ATCC 10556, Streptococcus sanguis group H1, Neisseria subflava and Staphylococcus ) and adult human oral mucosa (AHOM) antigens were investigated in relation to exacerbation of recurrent aphthous stomatitis (RAS). The material consisted of 10 patients with RAS and 10 controls. The CMI and HI were assessed by means of the leukocyte migration test (LMT) and a double‐layer immunofluorescence (IF) technique. Compared with normal controls the leukocyte migration inhibition against Strep. 2A and AHOM was significantly increased in patients with exacerbation of RAS and the reactivity seemed to develop in relation to the exacerbation of RAS. The leukocyte migration inhibition was not significantly increased when Strep. H1, Neisseria subflava, Staphylococcus or fetal human kidney extracts were used as antigens. The IgG antibodies against Strep. 2A and Strep. H1 were significantly raised in sera from patients with exacerbation of RAS. However, the endpoint titers (EPT) did not increase significantly in relation to the exacerbation of RAS. The distribution of EPT against Neisseria subflava, Staphylococcus and AHOM did not differ significantly when sera from patients with exacerbation of RAS were related to sera from controls. The present investigations support the hypothesis that CMI against streptococcal and AHOM antigens may be involved in the immunopathogenesis of RAS.