Abstract
Recent attention has focused on the T helper type 2 (Th2) lymphocyte as a source of interleukin 4 (IL-4) in allergic disease. However, Th2 cells themselves require a pulse of IL-4 to initiate this synthesis. Here we provide immunohistochemical evidence of IL-4 localization to human mast cells of the skin and respiratory tract, and demonstrate that immunoglobulin E-dependent stimulation of purified human lung mast cells leads to the rapid release of IL-4 into the extracellular environment. We propose that mast cell activation in an allergic response provides a rapid and local pulse of IL-4 into the local environment essential for the triggering of T lymphocytes into sustained IL-4 production and to initiate inflammatory cell accumulation and activation.
Highlights
L4 is a multifunctional cytokine that appears to play an important role in the pathogenesis of allergic disease
The isotype switching of B cells to IgE synthesis is under the control of IL-4 (1), and in vivo IgE responses in mice are inhibited after prior administration of neutralizing
Specificity of immunostaining was demonstrated in Chinese hamster ovary (CHO) cells transfected with cDNA for human IL-4
Summary
We have used immunohistochemistry to study the presence and cellular localization of IL4 in situ in the human respiratory tract, validated the method in IL4 gene-transfected hamster CHO cells, supplemented our findings by immunostaining of purified human skin and lung mast cells for IL4, and demonstrated its release along with histamine from mast cells with IgE-dependent activation . Mouse IgG1 mAbs 384 and 4139 to human [11,4] (12), AA1 to mast cell tryptase, antiCD3, and anti-CD4 were applied to sequential sections.
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