IL-6 production by human T lymphocytes. Expression in HTLV-1-infected but not in normal T cells.
 IL-6 is an important regulator of humoral and cellular immunity.
 Although this cytokine is produced by diverse cell types, it is not known whether it is produced by T lymphocytes under physiologic conditions or which agents can induce T cell expression of IL-6.
 We analyzed the production of IL-6 by human peripheral blood T cells, human thymocytes, and human T cell lines.
 In pure populations of these cells, stimulated with different combinations of various mitogens and cytokines, IL-6 activity could not be detected.
 Analysis of purified T-alpha beta and T-gamma delta cells showed that neither T cell subset produced IL-6.
 Similarly, IL-6 mRNA was not detected in T cell or thymocyte populations for up to 48 h after stimulation.
 With the use of a PCR assay, IL-6 mRNA in T cells was found to be virtually negligible, and did not change after T cell activation.
 By in situ hybridization it was shown that the cells expressing IL-6 mRNA after mitogen activation of PBMC do not belong to the T cell lineage.
 To analyze whether human T cells express IL-6 in vivo, we examined lymphoid tissues by in situ hybridization.
 In normal human thymus there was no detectable signal for IL-6.
 Tonsils showed only few positive cells within the parenchyma, but strong expression of IL-6 by epithelial cells in crypts.
 In contrast to normal lymph node, which contained only rare cells positive for IL-6, a lymph node from a patient with Castleman's disease showed IL-6 expression in cells occupying the marginal sinus and interfollicular areas.
 Screening of various human T cell lines showed that all cell lines infected with HTLV-1 secrete IL-6 activity and express IL-6 mRNA.
 In addition, in vitro infection of peripheral blood T cells with HTLV-1 induced de novo synthesis and secretion of IL-6.
 Furthermore, IL-6 expression in HTLV-1-infected cells was enhanced by stimulation with IL-1 beta or TNF-alpha.
 In contrast, IL-6 was not detectable in non-infected T cell lines.
 These studies indicate that IL-6 may not be a physiologic product of human T lymphocytes and that infection of T cells with HTLV-1 results in aberrant expression of this cytokine.
