Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis

T. Hibi, M. Ohara, M. Watanabe, Takanori Kanai, Hiromasa Takaishi, A. Hayashi, Y. Hosoda, Haruhiko Ogata, Yasushi Iwao, S. Aiso, N. Watanabe, K. Toda, M. Tsuchiya

研究成果: Article

12 引用 (Scopus)

抄録

In vitro effects of cytokines and therapeutic drugs on antibody dependent cellular cytotoxicity (ADCC) mediated by anticolon antibody were investigated in serum samples from patients with ulcerative colitis. A 51Cr release assay was used to examine ADCC activity with the colon cancer cell line, colo 205, as the target and peripheral blood mononuclear cells as the effector. High ADCC activity was shown in 13 of 32 (41%) patients with ulcerative colitis. This ADCC activity was inhibited by protein A treatment of the serum samples. Interleukin 2 (IL2) activated effector cells could enhance ADCC activity, but interferon-γ (IFN-γ) or tumour necrosis factor-α (TNF-α) had no effect on the cytotoxic activity of effector cells. Treatment of target cells with IFN-γ increased the vulnerability of these cells to ADCC with a large increase of intercellular adhesion molecule-1 (ICAM-1) expression on their surface. Monoclonal antibodies to ICAM-1 inhibited this IFN-γ enhanced ADCC activity. Interestingly, prednisolone (PSL) reduced ADCC activity, but sulphasalazine (SASP) or 5-aminosalicylic acid (5-ASA) did not. These results suggest that IL2 and IFN-γ could enhance colonic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.

元の言語English
ページ(範囲)788-793
ページ数6
ジャーナルGut
34
発行部数6
出版物ステータスPublished - 1993 6

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Ulcerative Colitis
Interferons
Interleukin-2
Antibodies
Intercellular Adhesion Molecule-1
Prednisolone
Cytokines
Mesalamine
Sulfasalazine
Staphylococcal Protein A
Therapeutic Uses
Serum
Colonic Neoplasms
Blood Cells
Therapeutics
Tumor Necrosis Factor-alpha
Epithelial Cells
Monoclonal Antibodies
Cell Line
Wounds and Injuries

ASJC Scopus subject areas

  • Gastroenterology

これを引用

Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis. / Hibi, T.; Ohara, M.; Watanabe, M.; Kanai, Takanori; Takaishi, Hiromasa; Hayashi, A.; Hosoda, Y.; Ogata, Haruhiko; Iwao, Yasushi; Aiso, S.; Watanabe, N.; Toda, K.; Tsuchiya, M.

:: Gut, 巻 34, 番号 6, 06.1993, p. 788-793.

研究成果: Article

Hibi, T, Ohara, M, Watanabe, M, Kanai, T, Takaishi, H, Hayashi, A, Hosoda, Y, Ogata, H, Iwao, Y, Aiso, S, Watanabe, N, Toda, K & Tsuchiya, M 1993, 'Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis', Gut, 巻. 34, 番号 6, pp. 788-793.
Hibi, T. ; Ohara, M. ; Watanabe, M. ; Kanai, Takanori ; Takaishi, Hiromasa ; Hayashi, A. ; Hosoda, Y. ; Ogata, Haruhiko ; Iwao, Yasushi ; Aiso, S. ; Watanabe, N. ; Toda, K. ; Tsuchiya, M. / Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis. :: Gut. 1993 ; 巻 34, 番号 6. pp. 788-793.
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abstract = "In vitro effects of cytokines and therapeutic drugs on antibody dependent cellular cytotoxicity (ADCC) mediated by anticolon antibody were investigated in serum samples from patients with ulcerative colitis. A 51Cr release assay was used to examine ADCC activity with the colon cancer cell line, colo 205, as the target and peripheral blood mononuclear cells as the effector. High ADCC activity was shown in 13 of 32 (41{\%}) patients with ulcerative colitis. This ADCC activity was inhibited by protein A treatment of the serum samples. Interleukin 2 (IL2) activated effector cells could enhance ADCC activity, but interferon-γ (IFN-γ) or tumour necrosis factor-α (TNF-α) had no effect on the cytotoxic activity of effector cells. Treatment of target cells with IFN-γ increased the vulnerability of these cells to ADCC with a large increase of intercellular adhesion molecule-1 (ICAM-1) expression on their surface. Monoclonal antibodies to ICAM-1 inhibited this IFN-γ enhanced ADCC activity. Interestingly, prednisolone (PSL) reduced ADCC activity, but sulphasalazine (SASP) or 5-aminosalicylic acid (5-ASA) did not. These results suggest that IL2 and IFN-γ could enhance colonic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.",
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AU - Hibi, T.

AU - Ohara, M.

AU - Watanabe, M.

AU - Kanai, Takanori

AU - Takaishi, Hiromasa

AU - Hayashi, A.

AU - Hosoda, Y.

AU - Ogata, Haruhiko

AU - Iwao, Yasushi

AU - Aiso, S.

AU - Watanabe, N.

AU - Toda, K.

AU - Tsuchiya, M.

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