PMID- 9119966
OWN - NLM
STAT- MEDLINE
DCOM- 19970424
LR  - 20190826
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 74
IP  - 1-2
DP  - 1997 Apr
TI  - gamma delta T-cell-human glial cell interactions. I. In vitro induction of 
      gammadelta T-cell expansion by human glial cells.
PG  - 135-42
AB  - gamma delta T-cells are found in increased proportion in multiple sclerosis (MS) 
      white matter plaque infiltrates compared with peripheral blood or spleen, raising 
      the possibility that they are either specifically attracted to lesion sites or, 
      once present, are stimulated to expand. We have previously shown that human 
      oligodendrocytes (OGC) preferentially express heat shock proteins (hsp), 
      molecules to which gamma delta T-cells have been known to react and that in vitro 
      expanded gamma delta T-cells can lyse OGC. We therefore investigated whether 
      human glial cells, that differentially express hsp, could stimulate gamma delta 
      T-cell expansion from peripheral blood. We compared the glial cell-induced 
      expansion to cell lines which also differentially express hsp and have been shown 
      to selectively stimulate gamma delta T-cell expansion (e.g. RPMI 8226, Daudi). We 
      found that both OGC and human fetal astrocytes (hFA) expressed hsp and stimulated 
      the preferential expansion of gamma delta T-cells to about the same extent as the 
      hsp expressing cell lines RPMI 8226 or Daudi, in the presence of exogenous 
      interleukin-2 (IL-2) but without any T-cell mitogen. Furthermore, the type of 
      gamma delta T-cells expanded were of the V delta 2 subtype known to be 
      particularly reactive to hsp. Microglia, U937 cell lines or purified myelin 
      membranes, which express little or no hsp, did not support gamma delta T-cell 
      growth. These results therefore suggest that OGC may contribute to the local 
      expansion of gamma delta T-cells within MS plaques. Potential harmful effects of 
      gamma delta T-cells on OGC may thereby contribute to the immunopathogenesis of MS 
      demyelination.
FAU - Freedman, M S
AU  - Freedman MS
AD  - University of Ottawa, Department of Medicine, Ont., Canada. mfreedman@ogh.on.ca
FAU - D'Souza, S
AU  - D'Souza S
FAU - Antel, J P
AU  - Antel JP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Chaperonin 60)
RN  - 0 (Receptors, Antigen, T-Cell, gamma-delta)
SB  - IM
MH  - Astrocytes/metabolism
MH  - *Cell Communication
MH  - Cell Division
MH  - Cell Line/physiology
MH  - Chaperonin 60/metabolism
MH  - Fetus/cytology/metabolism
MH  - Humans
MH  - Neuroglia/metabolism/*physiology
MH  - Oligodendroglia/metabolism
MH  - Phenotype
MH  - Receptors, Antigen, T-Cell, gamma-delta/*metabolism
MH  - T-Lymphocytes/*physiology
EDAT- 1997/04/01 00:00
MHDA- 2000/06/01 09:00
CRDT- 1997/04/01 00:00
PHST- 1997/04/01 00:00 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1997/04/01 00:00 [entrez]
AID - S0165-5728(96)00217-2 [pii]
AID - 10.1016/s0165-5728(96)00217-2 [doi]
PST - ppublish
SO  - J Neuroimmunol. 1997 Apr;74(1-2):135-42. doi: 10.1016/s0165-5728(96)00217-2.