Correlation between phenotypic characteristics of mononuclear cells isolated from human periapical lesions and their in vitro production of Th1 and Th2 cytokines
“…In addition, the number of IL-17-positive cells increased during the lesion expansion periods. The lymphocyte was the predominant IL-17-positive cell type, which agrees with previous findings that T lymphocytes were the predominant inflammatory cells infiltrating periradicular lesions (21) and that IL-17 is produced almost exclusively by activated T cells (9). Our results were also in accordance with Colić et al (26) who found that mononuclear cells, isolated from periapical lesions, produce significant amounts of IL-17 upon additional stimulation, and the IL-17 concentration correlated with the proportion of CD3ϩ and CD4ϩ cells.…”
Section: Discussionsupporting
confidence: 90%
“…These lesions are characterized by the persistent migration and infiltration of inflammatory cells such as neutrophils, lymphocytes, plasma cells, macrophages, and mast cells (20). Previous investigations have suggested that CD4 ϩ T lymphocytes are the predominant inflammatory cells that infiltrate the pathogenesis of periapical lesions and play a key role in the disease (21,22). IL-17A is a proinflammatory cytokine that is primarily secreted from T lymphocytes, mediators of adaptive immunity.…”
“…In addition, the number of IL-17-positive cells increased during the lesion expansion periods. The lymphocyte was the predominant IL-17-positive cell type, which agrees with previous findings that T lymphocytes were the predominant inflammatory cells infiltrating periradicular lesions (21) and that IL-17 is produced almost exclusively by activated T cells (9). Our results were also in accordance with Colić et al (26) who found that mononuclear cells, isolated from periapical lesions, produce significant amounts of IL-17 upon additional stimulation, and the IL-17 concentration correlated with the proportion of CD3ϩ and CD4ϩ cells.…”
Section: Discussionsupporting
confidence: 90%
“…These lesions are characterized by the persistent migration and infiltration of inflammatory cells such as neutrophils, lymphocytes, plasma cells, macrophages, and mast cells (20). Previous investigations have suggested that CD4 ϩ T lymphocytes are the predominant inflammatory cells that infiltrate the pathogenesis of periapical lesions and play a key role in the disease (21,22). IL-17A is a proinflammatory cytokine that is primarily secreted from T lymphocytes, mediators of adaptive immunity.…”
“…In contrast, periapical cysts were characterized by a Th1 and Th2 response, with increased IFN- γ , TNF- α , and IL-4 levels which were correlated to clinical evidence of swelling and tenderness to percussion [46]. Other studies suggest that Th1 response is predominant in apical granulation tissues, while Th2 response is dominant in human periapical regenerating lesions [21, 47]. On the other hand, experimental models suggest a hierarchy of Th2 cytokines in the immunomodulation of apical periodontitis, given that the absence of Th1-type cytokines (IFN- γ and IL-12) does not interfere with the lesion development [23, 24], whereas the deficiency of Th2 cytokines, IL-6 [20] and IL-10 [23, 48], increases the extension of apical lesions.…”
Section: Il-12-related Immune Responses In Periapical Lesionsmentioning
Periapical lesions are inflammatory conditions of tooth periapical tissues, triggered by dental pulp infection and characterized by exudation of immune cells to the affected tissues and production of inflammatory mediators such as cytokines. The inflammatory periapical reaction is mainly driven by Th1, Th2, and Th17 responses, and such polarization may modulate progression of the disease and expression of bone proresorptive cytokines. IL-12 is a potent inducer of IFN-γ production, which stimulates Th1 effector cells. Many evidences have shown a positive correlation between the bone resorptive cytokine IL-1β and the production of IL-12 and IFN-γ. Furthermore, IL-12 may have a potential role in the release of bone resorptive mediators and blockade of Th2 cytokines, affecting the progression of periapical bone loss. Nevertheless, IL-12 and IFN-γ have also been described as suppressors of osteoclast differentiation and activation, favoring bone maintenance. This paper focuses on the controversial roles of IL-12 in periapical lesions.
“…22 IL-12 induces the production of IFN-γ, thereby increasing the cytotoxic capacity of CD57 + NK cells. 27 Sabeti et al 6 analyzed the presence of EBV and HCMV and the expression of different cytokines, including IL-12, in periapical lesions. Using polymerase chain reaction (PCR), the authors observed significant correlations between infection with EBV and HCMV and the expression of some cytokines such as IL-12.…”
The aim of this study was to compare the number of CD57 + natural killer (NK) cells and CD8 + T lymphocytes between periapical granulomas (PGs) and radicular cysts (RCs). Twenty-fives cases of PGs and 25 of RCs were submitted to histological analysis and immunohistochemistry using anti-CD57 and anti-CD8 biomarkers. Positive cells were counted in 10 fields (400× magnification) and the median value was calculated for each case. Statistical tests were used to evaluate differences in the number of CD57+ NK cells and CD8 + T lymphocytes according to type of lesion, intensity of the infiltrate and thickness of the lining epithelium. The number of CD57 + NK cells and CD8 + T lymphocytes was higher in PGs than in RCs (p = 0.129 and p = 0.541, respectively). Comparison of the number of CD57 + NK cells in atrophic and hyperplastic epithelium revealed a larger number of cells in the atrophic epithelium (p = 0.042). A larger number of CD57 + NK cells and CD8 + T lymphocytes were observed in grade III infiltrates compared to grade I/II (p = 0.145 and p = 0.725, respectively). CD8 + T lymphocytes were more prevalent than CD57 + NK cells in most cases when PGs and RCs were analyzed separately or in combination (p < 0.0001). CD57+ NK cells and CD8 + T lymphocytes play a key role in antiviral defense and the presence of these cells supports evidence suggesting the participation of these microorganisms in the pathogenesis of PGs and RCs. The response mediated by CD8 + T lymphocytes was more frequent, indicating greater participation of the adaptive immunity in these chronic lesions.
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