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Accessory cells induce a polyphosphatidylinositol response when cultured with mitogen‐activated T lymphocytes
Author(s) -
Akeson Ann L.,
Mitani Kiminobu,
McCarthy Becky M.,
Harmony Judith A. K.
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041450222
Subject(s) - phosphatidylinositol , diacylglycerol kinase , interleukin 2 , second messenger system , microbiology and biotechnology , biology , concanavalin a , t lymphocyte , t cell , dna synthesis , inositol phosphate , lymphokine , inositol , biochemistry , kinase , protein kinase c , receptor , immune system , immunology , dna , in vitro
Abstract Monocytes (MO) influenced phosphoinositide metabolism when human T lymphocytes, isolated from peripheral blood, were activated by polyclonal mitogens. In the 3 hr immediately following mitogenic challenge, the synthesis of phosphatidylinositol (PI) was augmented and the synthesis of PI‐4‐phosphate (PIP) and PI‐4,5‐bisphosphate (PIP 2 ) was induced in cultures of T lymphocytes and MO. In addition, MO induced a rapid and transient degradation of PIP and PIP 2 in T cells prelabeled with [ 32 P]PL and subsequently activated by mitogen. Induction of a PIP/PIP 2 response correlated well with induction of DNA replication by MO when T cells were activated by phytohemagglutinin or by neuraminidase plus galactose oxidase. MO did not influence polyphosphoinositide metabolism when T cells were stimulated by the nonmitogenic lectin wheat germ agglutinin. Interleukin 1 could not substitute for monocytes in inducing a polyphosphoinositide response. By causing a rapid and transient release of the second messengers diacylglycerol and inositol phosphates and by subsequently increasing their cellular precursors, MO may induce the interleukin 2 responsive state in T lymphocytes.