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Analysis of different protein kinase C‐dependent events in T cells from allogeneic bone marrow transplantation recipients
Author(s) -
BALBOA M. A.,
IZQUIERDO M.,
SANCHEZMADRID F.,
FERNÁNDEZRAÑADA J. M.,
LÓPEZBOTET M.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb03023.x
Subject(s) - immunology , transplantation , bone marrow transplantation , bone marrow , biology , medicine , cancer research
SUMMARY In order to understand the mechanisms underlying the T lymphocyte dysfunction associated to allogeneic bone marrow transplantation (BMT), we assessed two different protein kinase C (PKC) dependent events in T cells from BMT recipients: the PKC‐dependent membrane expression and function of the CD69 early activation antigen; and the rapid phorbol ester‐induced phosphorylation of PKC protein substrates in lysales from T cells permeabilized with digitonin, in the presence of (γ‐ 32 P)ATP. Most BMT recipient T cells detectably expressed the CD69 surface antigen after 24 h of stimulation with either phorbol 12‐myristate 13‐acetate (PMA) or anti‐CD3 MoAb and PMA, thus indicating that PKC activity is sufficient to induce de novo gene expression. Nevertheless, it is noteworthy that the fluorescent staining intensity with anti‐CD 69 ) MoAbs was significantly lower in BMT recipient T cells than in normal T lymphocytes, although no clear‐cut correlation was found between the expression of CD69 and the proliferative capacity. However, the pattern of PMA‐induced phosphoproteins analysed as early as 1 min after PKC activation in T cells from BMT recipients displaying a low response to mitogenic stimuli, was undistinguishablc from that detected in T cells from healthy subjects. In all cases a major 110‐kD phosphoprotein was observed, which was inducible with PMA. phorbol 12,13‐dibutyrate (PDBu). 1‐oleoyl‐2‐acetylglycerol (OAG) and a phorbol‐ester‐related activator of PKC (mezerein); moreover, its phosphorylation was blocked by pretreating cells with the PKC inhibitor H‐7. Altogether our results suggest that the depressed mitogenic responses, which were also observed in the present study when T cells were stimulated via CD69, cannot be simply attributed to a defective PKC activity.

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