The proliferative response of human T-lymphocyte clones, (TLC) specific for self-major histocompatibility complex (MHC) products either alone or associated with PPD epitopes are inhibited in vitro by dexamethasone (DEX) and by a non-specific inhibitory factor(s) (nsINH) produced by PPD-activated T-cells. The inhibiting effect has been investigated by preincubating autoreactive and PPD-specific TLC with nsINH or DEX. Results obtained indicate that T-lymphocytes are the target of these two immunoregulatory molecules. Moreover, the addition of exogenous recombinant interleukin 2 (rIL-2) substantially reverses the inhibition observed in both nsINH- or DEX-treated cultures.
Regulation of self-major histocompatibility complex reactive human T-cell clones / GILARDINI MONTANI, MARIA SAVERIA; F., DEL GALLO; M., Gobbi; G., Lombardi; Piccolella, Enza; O., Pugliese; V., Colizzi. - In: INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY. - ISSN 0192-0561. - STAMPA. - 12:3(1990), pp. 255-260.
Regulation of self-major histocompatibility complex reactive human T-cell clones.
GILARDINI MONTANI, MARIA SAVERIA;PICCOLELLA, Enza;
1990
Abstract
The proliferative response of human T-lymphocyte clones, (TLC) specific for self-major histocompatibility complex (MHC) products either alone or associated with PPD epitopes are inhibited in vitro by dexamethasone (DEX) and by a non-specific inhibitory factor(s) (nsINH) produced by PPD-activated T-cells. The inhibiting effect has been investigated by preincubating autoreactive and PPD-specific TLC with nsINH or DEX. Results obtained indicate that T-lymphocytes are the target of these two immunoregulatory molecules. Moreover, the addition of exogenous recombinant interleukin 2 (rIL-2) substantially reverses the inhibition observed in both nsINH- or DEX-treated cultures.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.