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Relationship between regulatory and type 1 T cells in dogs with oral malignant melanoma
Author(s) -
Horiuchi Yutaka,
Tominaga Makiko,
Ichikawa Mika,
Yamashita Masao,
Okano Kumiko,
Jikumaru Yuri,
Nariai Yoko,
Nakajima Yuko,
Kuwabara Masato,
Yukawa Masayoshi
Publication year - 2010
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2009.00194.x
Subject(s) - melanoma , cd8 , peripheral blood , peripheral blood mononuclear cell , biology , immunity , stage (stratigraphy) , immunology , medicine , pathology , immune system , cancer research , paleontology , biochemistry , in vitro
Recent data suggest a decreased prevalence of IFN‐γ‐producing T lymphocytes (Type 1 T cells) in tumor‐bearing hosts. Moreover, it has been reported that Treg have a strong impact on the activation and proliferation of CD4 (+) and CD8 (+) lymphocytes; however, no previous reports have described the relationship between Treg and the progression of tumor, or Type 1 T cell populations in dogs with malignant tumor. In this study, the percentage of Treg, Th1, and Tc1 in the peripheral blood of dogs with oral malignant melanoma and healthy dogs was measured and compared. Although the percentages of Th1 and Tc1 in dogs with oral malignant melanoma were less than those in healthy dogs (Th1: P < 0.01, Tc1: P < 0.05), the percentage of Treg was increased ( P < 0.01). A significant inverse correlation between the percentage of Tc1 and the clinical tumor stage ( P < 0.01), and a significant correlation between that of Treg and the clinical tumor stage ( P < 0.001) was found. Moreover, there was a significant inverse correlation between the percentages of Treg and Th1 ( P < 0.05) or Tc1 ( P < 0.001). In conclusion, the percentage of Treg increases with the tumor stage in the peripheral blood of dogs with oral malignant melanoma. In dogs, Treg appears to suppress Type 1 immunity, which may be responsible for anti‐tumor responses.