Group I mGlu receptor stimulation inhibits activation-induced cell death of human T lymphocytes

Annalisa Chiocchetti, Gianluca Miglio, Riccardo Mesturini, Federica Varsaldi, Marco Mocellin, Elisabetta Orilieri, Chiara Dianzani, Roberto Fantozzi, Umberto Dianzani, Grazia Lombardi

Risultato della ricerca: Contributo su rivistaArticolo in rivistapeer review

Abstract

1. The effects of L-glutamate on activation-induced cell death (AICD) of human activated (1 μg ml -1 phytohemagglutinin plus 2 U ml -1 interleukin-2; 8 days) T lymphocytes were studied by measuring anti-CD3 monoclonal antibody (10 μg ml -1; 18 h)-induced cell apoptosis (Annexin V and propidium iodide staining). 2. L-Glutamate (1 × 10 -8-1 × 10 -4 M) significantly (P≤0.01) inhibited AICD in a concentration-dependent manner (EC 50=6.3 × 10 -8 M; maximum inhibition 54.8±6.3% at 1 × 10 -6 M). 3. The L-glutamate inhibitory effect was pharmacologically characterized as mediated by group I mGlu receptors, since mGlu receptor agonists reproduced this effect. The EC 50 values were: 3.2 × 10 -7 M for (1S,3R)-ACPD; 4.5 × 10 -8 M for quisqualate; 1.0 × 10 -6 M for (S)-3,5-DHPG; 2.0 × 10 -5 M for CHPG. 4. Group I mGlu receptor antagonists inhibited the effects of quisqualate 1.0 × 10 -6 M. The IC 50 values calculated were: 8.7 × 10 -5, 4.3 × 10 -6 and 6.3 × 10 -7 M for AIDA, LY 367385 and MPEP, respectively. 5. L-Glutamate (1 × 10 -6 M; 18 h) significantly (P≤0.05) inhibited FasL expression (40.8±11.3%) (cytofluorimetric analysis), whereas it did not affect Fas signalling. 6. Expression of both mGlu 1 and mGlu 5 receptor mRNA by T lymphocytes and T-cell lines, as demonstrated by reverse transcriptase-PCR analysis, suggests that L-glutamate-mediated inhibition of AICD was exerted on T cells. 7. These data depict a novel role for L-glutamate in the regulation of the immune response through group I mGlu receptor-mediated mechanisms.

Lingua originaleInglese
pagine (da-a)760-768
Numero di pagine9
RivistaBritish Journal of Pharmacology
Volume148
Numero di pubblicazione6
DOI
Stato di pubblicazionePubblicato - 22 lug 2006

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