PMID- 15145213
OWN - NLM
STAT- MEDLINE
DCOM- 20040624
LR  - 20191210
IS  - 0301-472X (Print)
IS  - 0301-472X (Linking)
VI  - 32
IP  - 5
DP  - 2004 May
TI  - Codevelopment of dendritic cells along with erythroid differentiation from human 
      CD34(+) cells by tumor necrosis factor-alpha.
PG  - 450-60
AB  - OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) inhibits erythropoiesis and 
      enhances nonerythroid colony formation. The present study examines the nature of 
      these nonerythroid cells and investigates their physiologic role in relation to 
      erythroid progenitor cells. MATERIALS AND METHODS: Highly purified human CD34(+) 
      cells underwent erythroid differentiation in the presence of multiple cytokines, 
      including stem cell factor (SCF), interleukin-3 (IL-3), and erythropoietin (EPO), 
      with and without TNF-alpha. We enumerate colony-forming unit-erythroid (CFU-E) 
      and glycophorin A (GPA; a specific marker for erythroid lineage) positive cells 
      in semisolid phase as well as in liquid suspension culture. The character and 
      roles of codeveloping nonerythroid cells in the presence of TNF-alpha were 
      analyzed using fluorescent activating cell sorter, enzyme immunohistochemistry, 
      and confocal microscopy. RESULTS: TNF-alpha inhibited the generation of GPA(+) 
      cells and conversely enhanced the generation of GPA(-) cells. The GPA(-) cells 
      were comprised of cells with excentric cell shape and were positive for HLA class 
      I, HLA class II, CD1a, CD4, CD11c, CD14, CD40, CD80, CD83, and CD86, but not for 
      CD3, CD8, CD19, CD20, and CD56, indicating the codevelopment of dendritic cells 
      (DC) along with erythroid differentiation. Developing DC/DC precursors were 
      detected within 3 days of culture. Only in the presence of TNF-alpha did CD34(+) 
      cells proliferate by forming aggregates where both GPA(+) and CD11c(+) DC/DC 
      precursors were present. During culture period, immature CD11c(+) DC were capable 
      of endocytosing damaged GPA(+) cells. CONCLUSIONS: GPA(-) cells cogenerated from 
      human CD34(+) cells during erythroid differentiation in the presence of 
      IL-3/SCF/EPO and TNF-alpha express DC phenotypes. The CD11c(+) DC subset 
      physically and selectively associates with developing immature erythroid cells 
      and damaged self-GPA(+) cells and then obtains and captures self-substances.
FAU - Fukaya, Hiroshi
AU  - Fukaya H
AD  - Department of Animal Development and Physiology, Graduate School of Biostudies, 
      Kyoto University, Kyoto, Japan.
FAU - Xiao, Weiguo
AU  - Xiao W
FAU - Inaba, Kayo
AU  - Inaba K
FAU - Suzuki, Yoshiko
AU  - Suzuki Y
FAU - Hirokawa, Makoto
AU  - Hirokawa M
FAU - Kawabata, Yoshinari
AU  - Kawabata Y
FAU - Komatsuda, Atsushi
AU  - Komatsuda A
FAU - Endo, Tomoyuki
AU  - Endo T
FAU - Kishimoto, Hiroyuki
AU  - Kishimoto H
FAU - Takada, Goro
AU  - Takada G
FAU - Sawada, Kenichi
AU  - Sawada K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Exp Hematol
JT  - Experimental hematology
JID - 0402313
RN  - 0 (Antigens, CD34)
RN  - 0 (CD11c Antigen)
RN  - 0 (Cytokines)
RN  - 0 (Glycophorins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - *Antigens, CD34
MH  - CD11c Antigen/analysis
MH  - Cell Adhesion
MH  - Cell Culture Techniques/methods
MH  - Cell Differentiation/drug effects
MH  - Cell Size
MH  - Cytokines/pharmacology
MH  - Dendritic Cells/*cytology
MH  - Erythroid Cells/*cytology
MH  - Glycophorins/analysis
MH  - Humans
MH  - Immunophenotyping
MH  - Inflammation/pathology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2004/05/18 05:00
MHDA- 2004/06/25 05:00
CRDT- 2004/05/18 05:00
PHST- 2003/12/08 00:00 [received]
PHST- 2004/02/17 00:00 [revised]
PHST- 2004/02/23 00:00 [accepted]
PHST- 2004/05/18 05:00 [pubmed]
PHST- 2004/06/25 05:00 [medline]
PHST- 2004/05/18 05:00 [entrez]
AID - S0301472X04000682 [pii]
AID - 10.1016/j.exphem.2004.02.011 [doi]
PST - ppublish
SO  - Exp Hematol. 2004 May;32(5):450-60. doi: 10.1016/j.exphem.2004.02.011.