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 colinic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.
| Original language | English |
|---|---|
| Pages (from-to) | 788-793 |
| Number of pages | 6 |
| Journal | Gut |
| Volume | 34 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 1993 Jan 1 |
| Externally published | Yes |
ASJC Scopus subject areas
- Gastroenterology
Cite this
Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis. / Hibi, T.; Ohara, M.; Watanabe, M.; Kanai, T.; Takaishi, H.; Hayashi, A.; Hosoda, Y.; Ogata, H.; Iwao, Y.; Aiso, Sadakazu; Watanabe, N.; Toda, K.; Tsuchiya, M.
In: Gut, Vol. 34, No. 6, 01.01.1993, p. 788-793.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Interleukin 2 and interferon-γ augment anticolon antibody dependent cellular cytotoxicity in ulcerative colitis
AU - Hibi, T.
AU - Ohara, M.
AU - Watanabe, M.
AU - Kanai, T.
AU - Takaishi, H.
AU - Hayashi, A.
AU - Hosoda, Y.
AU - Ogata, H.
AU - Iwao, Y.
AU - Aiso, Sadakazu
AU - Watanabe, N.
AU - Toda, K.
AU - Tsuchiya, M.
PY - 1993/1/1
Y1 - 1993/1/1
N2 - 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 colinic epithelial cell injury mediated by the ADCC mechanism in ulcerative colitis and that ADCC enhanced by cytokines is restored by PSL treatment.
AB - 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 colinic 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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U2 - 10.1136/gut.34.6.788
DO - 10.1136/gut.34.6.788
M3 - Article
VL - 34
SP - 788
EP - 793
JO - Gut
JF - Gut
SN - 0017-5749
IS - 6
ER -