TY - JOUR
T1 - Additive effect of interleukin-12 and interleukin-18 on the T-helper cell pathway of malignant pleural effusion
AU - Yao, N. S.
AU - Chen, Y. M.
AU - Perng, R. P.
AU - Whang-Peng, J.
N1 - Funding Information:
Dr. Albert receives research funding from Aetna Inc.
Funding Information:
This work was supported by a Pfizer Medical Education Group grant and the Columbia University Center for New Media Teaching and Learning Initiative.
PY - 2002/12/1
Y1 - 2002/12/1
N2 - Interleukin-18 (IL-18) is a novel cytokine with interferon-γ (IFN-γ)-inducing activity, thus favoring the T-helper type 1 (Th-1) pathway. The present study attempts to define the role of IL-18 on the functions of lymphocytes isolated from malignant pleural effusions (EAL, effusion-associated lymphocytes). EAL from 10 patients with malignant pleural effusion were incubated with IL-2, IL-12, or IL-18 with/without a αCD3 antibody. ELISA, proliferation, and cytotoxicity assays were performed. IL-18 alone was found to have no significant effect on EAL in terms of cytokine production, lymphocyte proliferation, or cytotoxicity against tumor targets. IL-18 also had no significant additive or synergistic effect on IL-2, IL-12, or αCD3 co-cultured EAL. However, when IL-18 was used with IL-12, the highest IFN-γ/IL-10 ratio was derived, suggesting that these two cytokines had an additive effect in leading EAL from the Th-2 to the Th-1 pathway. Furthermore, 1 of 5 patients' EAL had its strongest cytolytic activity against an autologous tumor when the EAL was cultured with IL-2 plus IL-18, as compared with the other 4 patients whose EAL cytolytic activity against autologous tumor was highest when using IL-2 plus αCD3. These findings suggest that IL-18 alone did not have a significant effect on EAL, and that IL-18 did not enhance αCD3's activity on EAL. However, its additive effect with IL-12 in the Th-1 pathway and with IL-2 in its cytolytic activity against an autologous tumor deserve further studies.
AB - Interleukin-18 (IL-18) is a novel cytokine with interferon-γ (IFN-γ)-inducing activity, thus favoring the T-helper type 1 (Th-1) pathway. The present study attempts to define the role of IL-18 on the functions of lymphocytes isolated from malignant pleural effusions (EAL, effusion-associated lymphocytes). EAL from 10 patients with malignant pleural effusion were incubated with IL-2, IL-12, or IL-18 with/without a αCD3 antibody. ELISA, proliferation, and cytotoxicity assays were performed. IL-18 alone was found to have no significant effect on EAL in terms of cytokine production, lymphocyte proliferation, or cytotoxicity against tumor targets. IL-18 also had no significant additive or synergistic effect on IL-2, IL-12, or αCD3 co-cultured EAL. However, when IL-18 was used with IL-12, the highest IFN-γ/IL-10 ratio was derived, suggesting that these two cytokines had an additive effect in leading EAL from the Th-2 to the Th-1 pathway. Furthermore, 1 of 5 patients' EAL had its strongest cytolytic activity against an autologous tumor when the EAL was cultured with IL-2 plus IL-18, as compared with the other 4 patients whose EAL cytolytic activity against autologous tumor was highest when using IL-2 plus αCD3. These findings suggest that IL-18 alone did not have a significant effect on EAL, and that IL-18 did not enhance αCD3's activity on EAL. However, its additive effect with IL-12 in the Th-1 pathway and with IL-2 in its cytolytic activity against an autologous tumor deserve further studies.
KW - Interferon-γ
KW - Interleukin-12
KW - Interleukin-18
KW - Interleukin-2
KW - Malignant effusion
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U2 - 10.1007/s004080000077
DO - 10.1007/s004080000077
M3 - Article
C2 - 12105753
AN - SCOPUS:0036901999
SN - 0341-2040
VL - 180
SP - 15
EP - 24
JO - Pneumonologie. Pneumonology
JF - Pneumonologie. Pneumonology
IS - 1
ER -