Macrophage inflammatory protein-1α (MIP-1α) is a member of the intercrine/chemokine family which consists of basic, heparin-binding, small molecular weight proteins. We have previously shown that a T cell line, CTLL- R8, carried high-affinity receptors for MIP-1α and the proliferation of CTLL-R8 cells was inhibited by murine recombinant (mr) MIP-1α. We extended our previous studies to murine resting splenic T lymphocytes to determine whether the inhibition of T cell proliferation is a general property of MIP- 1α. The resting splenic T cells carried approximately 680 high-affinity binding sites for mrMIP-1α; more than 90% of the primary T cells carried MIP-1α receptors. When the T cells were stimulated with immobilized anti- CD3 mAb in the presence of accessory cells, the MIP-1α binding was reduced. The lowest binding was obtained 2 h after anti-CD3 mAb stimulation due to the internalization of MIP-1α receptors. mrMIP-1α inhibited the anti-CD3 mAb- mediated proliferation of murine splenic T lymphocytes. The maximum inhibition was obtained when mrMIP-1α was added 30 min before anti-CD3 mAb stimulation. Slight inhibition of T cell proliferation was observed when mrMIP-1α was added at the same time as anti-CD3 mAb stimulation. These results indicate that T lymphocytes are regulated negatively by MIP-1α, which occurs when the T cells are exposed to MIP-1α before activation. The negative effect of MIP-1α seems to be mediated in part by the inhibition of IL-2 production, for there was a reduction in both the IL-2 mRNA levels and the IL-2 activity in supernatants from T cells preincubated with MIP-1α before anti-CD3 mAb stimulation.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Immunology|
|State||Published - 1993|
ASJC Scopus subject areas
- Immunology and Allergy