Lck is involved in interleukin-2 induced proliferation but not cell survival in human T cells through a MAP kinase-independent pathway.
Eur Cytokine Netw
; 11(2): 225-31, 2000 Jun.
Article
en En
| MEDLINE
| ID: mdl-10903801
The role of Lck in IL-2-induced proliferation and cell survival is still controversial. Here, we show that the Src family kinase inhibitor, PP1, reduced the IL-2-induced proliferation of human T cells significantly without inhibiting the anti-apoptotic effect of IL-2. As Lck is the only Src family kinase activated upon IL-2 stimulation in T cells, this indicates that Lck is involved in IL-2-induced proliferation but not survival. IL-2-induced MAP kinase activation was only slightly inhibited by PP1, suggesting that Lck is not essential for IL-2-induced MAP kinase activation in human T cells. We found that an IL-2-sensitive, human mycosis fungoides-derived tumor T cell line is Lck negative, and that the IL-2-induced MAP kinase activation is comparable to non-cancerous T cells, although a little delayed in kinetics. An Lck expressing clone was established by transfecting Lck into mycosis fungoides tumor T cells, but Lck had no influence on the delayed kinetics of MAP kinase activation, indicating that Lck is not essential for MAP kinase activation in mycosis fungoides tumor T cells or in non-cancerous T cells. Taken together, this indicates that Lck is involved in IL-2-induced proliferation, but not cell survival, through a pathway not involving MAP kinase.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Linfocitos T
/
Interleucina-2
/
Proteína Tirosina Quinasa p56(lck) Específica de Linfocito
Límite:
Humans
Idioma:
En
Revista:
Eur Cytokine Netw
Asunto de la revista:
ALERGIA E IMUNOLOGIA
Año:
2000
Tipo del documento:
Article
País de afiliación:
Dinamarca
Pais de publicación:
Francia