INTESTINAL INTRAEPITHELIAL LYMPHOCYTES - IDENTIFICATION OF AN INHIBITORY SUBPOPULATION

Citation
Dh. Teitelbaum et al., INTESTINAL INTRAEPITHELIAL LYMPHOCYTES - IDENTIFICATION OF AN INHIBITORY SUBPOPULATION, The Journal of surgical research, 63(1), 1996, pp. 123-127
Citations number
26
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
63
Issue
1
Year of publication
1996
Pages
123 - 127
Database
ISI
SICI code
0022-4804(1996)63:1<123:IIL-IO>2.0.ZU;2-P
Abstract
The intestinal intraepithelial lymphocytes (iIEL) may play a critical role in preventing overwhelming sensitization to foreign luminal antig ens. The purpose of this experiment was to identify the subpopulation of the iIEL responsible for this inhibitory action. One-way mixed lymp hocyte cultures (MLC) were performed with rat splenocytes [Brown Norwa y (BN) as responder; irradiated Lewis as stimulator]. BN iIEL (compris ing 5% of cells per well) were added to assess inhibitory function. In the control group, irradiated BN splenocytes were added to maintain i dentical cell numbers. Proliferation assays were expressed as mean cou nts per minute (CPM) +/- SD. Subpopulations of the iIEL were created b y biomagnetically extracting iIELs labeled with monoclonal antibodies, The addition of iIELs to the MLC resulted in a 59% reduction in proli feration (P < 0.05). When the CD45(+) population was removed from the iIEL this inhibitory activity was lost. Removal of the CD8(+) populati on, but not the CD4(+) population, also caused a loss of inhibitory ac tivity, Separate analysis of either CD8 alpha alpha(+) or CD8 alpha be ta(+) subpopulations identified the CD8 alpha alpha(+) population as h aving the majority of the inhibitory effect. In conclusion: 1) The iIE L has an inhibitory action on proliferation, 2) The involved populatio n is of lymphoid origin, as a loss of CD45(+) cells resulted in a loss of inhibition. 3) Loss of CD8(+) iIEL cells resulted in a loss of inh ibition demonstrating that these cells are responsible for this action . This inhibitory activity appears to be restricted to the CD8 alpha a lpha(+) subpopulation. (C) 1996 Academic Press, Inc.