PMID- 15596409
OWN - NLM
STAT- MEDLINE
DCOM- 20050215
LR  - 20061115
IS  - 1521-6616 (Print)
IS  - 1521-6616 (Linking)
VI  - 114
IP  - 1
DP  - 2005 Jan
TI  - Impaired function of circulating dendritic cells in patients with pancreatic 
      cancer.
PG  - 52-60
AB  - PURPOSE AND EXPERIMENTAL DESIGN: Dendritic cells (DCs) are important for immune 
      surveillance and play a central role in protection against infection and 
      malignancy. DCs comprise two subsets: DC1 (myeloid DC) and DC2 (lymphoid DC). The 
      aim of this study is to determine whether the number and/or function of 
      circulating DCs were decreased in patients with pancreatic cancer and to evaluate 
      the effects of these changes in patients with locally advanced pancreatic cancer 
      before and after chemoradiotherapy (CRT). We examined the circulating DC number 
      and function using the peripheral blood from 29 patients with pancreatic cancer 
      and 20 healthy control subjects. In patients who underwent CRT (n = 20), blood 
      samples were taken before and after CRT. DCs were tested for the ability to 
      stimulate allogeneic T lymphocytes in mixed leukocyte reaction (MLR). CD4/8, NK 
      activity, PHA, and TGF-beta1 were also measured. RESULTS: The number and 
      allostimulatory activity of circulating DC1s in patients were significantly lower 
      than those in controls. In the patients who underwent CRT, the allostimulatory 
      activity of DC1s at post-CRT was significantly increased as compared to those at 
      pre-CRT. The level of TGF-beta1 was also significantly decreased at post-CRT as 
      compared to pre-CRT. There were no changes in CD4/8, NK activity and 
      proliferative response of T lymphocytes at the peri-CRT period. CONCLUSION: These 
      data indicate that the number and function of circulating DCs were impaired in 
      patients with pancreatic cancer. Chemoradiotherapy, however, improved DC 
      function, which might be related to decreased immunosuppressive cytokine levels.
FAU - Yanagimoto, Hiroaki
AU  - Yanagimoto H
AD  - Department of Surgery, Kansai Medical University, Osaka, Japan. 
      yanagimh@takii.kmu.ac.jp
FAU - Takai, Soichiro
AU  - Takai S
FAU - Satoi, Sohei
AU  - Satoi S
FAU - Toyokawa, Hideyoshi
AU  - Toyokawa H
FAU - Takahashi, Kanji
AU  - Takahashi K
FAU - Terakawa, Naoyoshi
AU  - Terakawa N
FAU - Kwon, A-Hon
AU  - Kwon AH
FAU - Kamiyama, Yasuo
AU  - Kamiyama Y
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Clin Immunol
JT  - Clinical immunology (Orlando, Fla.)
JID - 100883537
RN  - 0 (Antineoplastic Agents)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Aged
MH  - Antineoplastic Agents/therapeutic use
MH  - Cell Count
MH  - Combined Modality Therapy
MH  - Dendritic Cells/*physiology
MH  - Female
MH  - HLA-DR Antigens/biosynthesis
MH  - Humans
MH  - Interleukin-12/biosynthesis
MH  - Lymphocyte Subsets
MH  - Male
MH  - Middle Aged
MH  - Pancreatic Neoplasms/*immunology/therapy
MH  - Transforming Growth Factor beta/blood
MH  - Transforming Growth Factor beta1
EDAT- 2004/12/15 09:00
MHDA- 2005/02/16 09:00
CRDT- 2004/12/15 09:00
PHST- 2004/05/15 00:00 [received]
PHST- 2004/09/22 00:00 [accepted]
PHST- 2004/12/15 09:00 [pubmed]
PHST- 2005/02/16 09:00 [medline]
PHST- 2004/12/15 09:00 [entrez]
AID - S1521-6616(04)00293-1 [pii]
AID - 10.1016/j.clim.2004.09.007 [doi]
PST - ppublish
SO  - Clin Immunol. 2005 Jan;114(1):52-60. doi: 10.1016/j.clim.2004.09.007.