Abstract
Immunological mechanisms participate in the pathogenesis of human chronic inflammatory periodontal disease (CIPD). Human CD4+ lymphocytes express functionally heterogeneous profiles of cytokine production. CD26 is an integral membrane glycoprotein, that is, a marker of Th1-like cytokine development. The purpose of the present study was to compare the immuno-expression of CD26 receptor in periodontal sites with and without clinical attachment loss (CAL). Five patients with rapidly progressing periodontitis and one with juvenile periodontitis were investigated. Each patient presented at least one site with and without CAL. Ten sites with CAL and nine without any CAL were biopsied, followed by the immunohistochemical identification of the CD26 receptor using the MIB-DS2/7 antibody. The results demonstrated that the percentage of positive cells for this antigen in the periodontal sites with CAL was not significantly different from those without attachment loss. Therefore, Th1 cell impairment may not be directly involved with periodontal attachment loss.
Highlights
Immunological mechanisms have been implicated in the pathogenesis of human chronic inflammatory periodontal disease (CPID) for over 30 years
Immunological mechanisms participate in the pathogenesis of human chronic inflammatory periodontal disease (CIPD)
The purpose of the present study was to compare the immuno-expression of CD26 receptor in periodontal sites with and without clinical attachment loss (CAL)
Summary
Immunological mechanisms have been implicated in the pathogenesis of human chronic inflammatory periodontal disease (CPID) for over 30 years. Defects in polymorphonuclear leukocytes [1], depressed cellular immune response [2, 3], polyclonal β-cell activation [4], and imbalance in the cytokine network [5,6,7,8,9,10] are some of the alterations reported. Few studies have compared immunological features of active versus nonactive periodontal lesions [11]. Human CD4+ lymphocytes express functionally heterogeneous profiles of cytokine production [12,13,14]. The same pattern of cytokine profile has been described in CD8+ lymphocytes. The Th1 subset induces cell-mediated immune responses, while the Th2 subset is associated with humoral-type responses
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