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Reduced CD8+ T cells infiltration can be associated to a malignant transformation in potentially malignant oral epithelial lesions.

Abstract：

OBJECTIVE:The aim of this study was to evaluate the immunohistochemical expressions of PD1, CD4+, and CD8+ in premalignant lesions (OPML) that were transformed into oral squamous cell carcinoma OSCC (OPML-OSCC), in OSCC and also in premalignant lesions that were not transformed into OSCC (OPML-NOSSC). MATERIALS AND METHODS:Retrospective analyses were performed in order to verify the demographic characteristics of the patients. CD4, CD8, and PD1 IMH studies were carried out on OPML and OSCC samples from 11 patients with OPML-OSCC and OPML, together with samples from 14 patients with OPML-NOSCC. The differences between OPML-OSCC and OPML-NOSCC were analyzed. RESULTS:Non-homogenous leukoplakia, together with the related oral subsite, and the lack of an exposure to tobacco, were all associated with malignant transformations. There were no statistical differences in the PD1 expression and the CD4+ cells in OPML-OSCC and OPML-NOSCC. A significant increment in the CD8+ cells was noted in the OPML that evolved into carcinomas when compared with OPML-NOSCC (p = 0.05), whereas there were higher CD8+ cells levels in the carcinomas when compared with the OPML that evolved into carcinomas (p = 0.027). CONCLUSIONS:CD8+ cells infiltrate more in OPML-NOSCC than in OPML-OSCC. Carcinoma is more infiltrated by CD8+ cells than its associated OPML. CLINICAL RELEVANCE:Understanding immunological factors associated with malignant transformation of oral premalignant lesions can open a new way to treat this disease.

journal_name

Clin Oral Investig

journal_title

Clinical oral investigations

authors

Chaves ALF,Silva AG,Maia FM,Lopes GFM,de Paulo LFB,Muniz LV,Dos Santos HB,Soares JMA,Souza AA,de Oliveira Barbosa LA,Loyola AM,Murta EFC,Michelin MA,de Azambuja Ribeiro RIM

doi

10.1007/s00784-018-2622-8

subject

Has Abstract

pub_date

2019-04-01 00:00:00

pages

1913-1919

issue

4

eissn

1432-6981

issn

1436-3771

pii

10.1007/s00784-018-2622-8

journal_volume

23

pub_type

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