PMID- 7635448
OWN - NLM
STAT- MEDLINE
DCOM- 19950913
LR  - 20190722
IS  - 0046-8177 (Print)
IS  - 0046-8177 (Linking)
VI  - 26
IP  - 8
DP  - 1995 Aug
TI  - Role of cytokines in distribution and differentiation of dendritic 
      cell/Langerhans' cell lineage in human primary carcinomas of the lung.
PG  - 866-72
AB  - The possibility that production of some cytokines in the carcinoma 
      microenvironment is associated with the presence and differentiation of cells 
      belonging to the dendritic cell (DC)/Langerhans' cell (LC) lineage was 
      investigated. Immunohistochemical examination showed the presence of 
      intraepithelial LCs (CD1a- and S100-positive cells) in 6 of 10 squamous cell 
      carcinomas and in 8 of 10 adenocarcinomas. Langerhans' cells were mainly located 
      close to lymphoid aggregates. In situ hybridization performed in four cases 
      (three LC positive and one LC negative) of squamous cell carcinoma and in five 
      cases (four LC positive and one LC negative) of adenocarcinoma showed that some 
      mononuclear cells in the interstitium displayed hybridization with granulocyte 
      macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF 
      alpha), and interleukin 1-beta (IL1 beta) cDNA probes. Only in LC-positive 
      carcinomas did epithelial cells close to lymphoid aggregates display small 
      amounts of GM-CSF and TNF alpha mRNA expression. Immunohistochemical analysis 
      performed in the 20 cases of lung carcinoma showed that epithelial cells in 
      tumors with lymphoid aggregates and LCs were immunoreactive with antihuman GM-CSF 
      monoclonal antibody. Specimens negative for GM-CSF contained very few LCs. 
      Northern blot analysis was used to investigate GM-CSF, TNF alpha, IL1 alpha, and 
      IL1 beta mRNA expression in six human lung carcinoma cell lines. A constitutive 
      expression of TNF alpha mRNA was found in all of them, whereas only three showed 
      a low constitutive expression of GM-CSF mRNA. In the latter three cell lines 
      treatment with phytohemagglutinin (PHA)-stimulated peripheral blood lymphocyte 
      (PBL) supernatant (PHA-SUP) upregulated GM-CSF mRNA expression and induced that 
      of IL1 alpha mRNA. Carcinomatous epithelial cells producing small amounts of 
      cytokines could promote the recruitment of cells of DC/LC lineage. Subcellular 
      factors produced by reactive lymphocytes and/or macrophages may influence the 
      production of GM-CSF and IL1 alpha by various epithelia. Up-regulation of this 
      production could favor the arrival and differentiation of DCs and activate LC 
      functions.
FAU - Colasante, A
AU  - Colasante A
AD  - Department of Human Pathology, G. D'Annunzio University, Chieti, Italy.
FAU - Castrilli, G
AU  - Castrilli G
FAU - Aiello, F B
AU  - Aiello FB
FAU - Brunetti, M
AU  - Brunetti M
FAU - Musiani, P
AU  - Musiani P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hum Pathol
JT  - Human pathology
JID - 9421547
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Adenocarcinoma/metabolism/*pathology
MH  - Carcinoma, Squamous Cell/metabolism/*pathology
MH  - Cell Differentiation
MH  - Cytokines/*physiology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/genetics/physiology
MH  - Humans
MH  - In Situ Hybridization
MH  - Interleukin-1/genetics/physiology
MH  - Langerhans Cells/*pathology
MH  - Lung Neoplasms/*metabolism/*pathology
MH  - RNA, Messenger/biosynthesis
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/genetics/physiology
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - 0046-8177(95)90009-8 [pii]
AID - 10.1016/0046-8177(95)90009-8 [doi]
PST - ppublish
SO  - Hum Pathol. 1995 Aug;26(8):866-72. doi: 10.1016/0046-8177(95)90009-8.