Mast cell desensitization to IgE fails to induce a parallel adenosine receptor desensitization.
Mast cell desensitization to IgE fails to induce a parallel adenosine receptor desensitization.
复制标题
肥大细胞对 IgE 的脱敏不能诱导平行的腺苷受体脱敏。
DOI：
10.1007/bf01976746
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Walker,LL
中科院分区：
文献类型：
--
作者：
Marquardt,DL;Lwin,A;Walker,LL
Desensitization induced by challenge of mast cells with antigen is specific for IgE-dependent signals. During the secretory process mast cells release adenosine, which can induce a desensitization of adenosine receptors. To determine whether adenosine receptors may de desensitized from a previous antigen challenge, mast cells were sensitized with anti-DNP IgE antibody, challenged with DNP-BSA antigen, returned to culture overnight, resensitized, and rechallenged. Previously challenged cells exhibited increased spontaneous β-hexosaminidase release, but adenosine retained its ability to augment β-hexosaminidase release. Adenosine enhanced A23187-stimulated release of β-hexosaminidase in control and previously challenged cells. Leukotriene C4generation followed a similar pattern. Mastoparan, a direct G protein activator and mast cells secretogogue, produced a doubling of β-hexosaminidase release in previously challenged cells. Results using other G protein activators were equivocal. Degranulation alone is insufficient to induce adenosine receptor hyposensitization. Whether the hyperresponsiveness to mastoparan is a consequence of uncoupling of IgE receptors from G proteins remains uncertain.
