We have previously reported that the T cell line Jurkat registers the exposure of a sinusoidal extremely low frequency magnetic field at the level of the plasma membrane, resulting in activation of the tyrosine kinase p56lck, increase in inositol‐3‐phosphate levels and increase in intracellular calcium concentration within minutes. To elucidate if these events associated with changes in intracellular calcium ion levels were biologically significant, transient transfections of Jurkat cells were performed with calcium‐ion dependent reporter constructs. Three different enhancer/promoter constructs were studied coupled to the luciferase reporter gene. The luciferase activity of each construct was measured after treatment of transfected cells to EMF exposure alone, or in combination with ionomycin, phorbol ester or cross‐linking anti‐CD3 antibodies. There was no indication that the used EMFs could influence any of these reporter constructs.

Jurkat E6-1 cells obtained from three different sources were compared with respect to intracellular calcium response to a 50 Hz, 0.15 mT, magnetic field, to treatment with poly-L-lysine and to protein expression at the cell surface. The fura-2 single cell measurements were a replication study performed by three members of our group. The cells responded to the applied magnetic fields, although the percentage of responding cells was lower than in earlier studies. The geomagnetic field was backed off without changing the outcome of the intracellular calcium measurements. Fluorometric analyses showed no difference between the E6-1 cells obtained from three sources with respect to the expression of cell surface marker molecules. The addition of the cell adhesive peptide, poly-L-lysine, did not itself cause any effects on the intracellular calcium concentration.

The human T cell line Jurkat registers a sinusoidal extremely low frequency (ELF), 0.10 mT magnetic fields (MFs) at the level of the plasma membrane. In this study, the protein tyrosine phosphorylation (PY) of two membrane-associated proteins in Jurkat cells were examined following a short-term MFs exposure, the ζ chains and the Src kinases p56lck. These proteins are interesting to study since the earliest biochemical event upon T cell receptor (TcR) activation is PY of the ζ chains. These signalling chains in the TcR complex was assessed using Western blotting and the activation of the p56lck kinase was analysed by in vitro kinase assay. The MFs exposure of Jurkat for 5 min activated p56lck and resulted in PY of ζ. These findings are in line with earlier reports on how MFs exposure affects signal transduction in Jurkat.

Extremely low frequency magnetic fields (MF) have been shown to alter the intracellular calcium concentration ([Ca2+]i) in the human leukemic T cell line Jurkat. Real-time [Ca2+]i oscillations were measured in different mutant Jurkat clones upon exposure to 50 Hz, 0.15 mT. A clone not expressing the T cell receptor α and β chains showed a reduced calcium response to MF compared to wild-type Jurkat (E6-1). A p56lck mutant clone showed a low response, which was restored when Lck was reconstituted, giving a response similar to that seen in E6-1 cells. The tyrosine phosphorylation intensity of immunoprecipitated Lck in E6-1 cells was higher in MF than sham-exposed cells. In addition, both cholera toxin (CTX) and the protein tyrosine kinase inhibitor genistein completely blocked the [Ca2+]i increase in Jurkat E6-1 cells upon MF exposure. Thus, MF affects the early events in a signalling pathway from the T cell receptor, although not exactly mimicking an anti-CD3-initiated [Ca2+]i response.

Low-frequency magnetic fields (MF) can increase the cytosolic calcium concentration ([Ca2+]i) in lymphocytes in the same manner as a physiological stimulus such as antibodies directed towards the CD3 complex. In this study, MF with various frequencies and flux densities were used, while [Ca2+]i changes were recorded using microfluorometry with fura-2 as a probe. The applied sinusoidal MF induced oscillatory changes of [Ca2+]i in the leukemic cell line Jurkat in a manner similar to that seen with stimulation by antibodies. The response at 0.15 mT was over a frequency range from 5 to 100 Hz, with a fairly broad peak having its maximum at 50 Hz. The result of testing increasing flux densities at 50 Hz was a threshold response with no effect below 0.04 mT and a plateau at 0.15 mT. On the basis of the characteristic calcium pattern resulting from an applied MF, we suggest that MF influence molecular events in regular signal transduction pathways of T cells.

We have earlier reported that when a weak 50 Hz MF (magnetic field) was applied, the leukemic T‐cell line Jurkat responded with intracellular calcium oscillations [Lindström, et al., J. Cell Physiol., 156 (1993) 395–398]. The result suggested that the MF interfered with the signal transduction, although neither target molecules nor molecular mechanisms are at present known. In this study we found that application of a MF to Jurkat cells resulted in significant increase of inositol 1,4,5‐trisphosphate (IP3) levels. Chelation of intracellular calcium ions by BAPTA/AM, did not block the increase of IP3 induced by MF. This result implied that MF‐induced Ca2+ oscillations were not due to direct stimulation of the Ca2+‐dependent phospholipase C‐γ1 (PLC‐γ1).

Oscillations of free intracellular calcium [Ca2+]i were seen in individual Jurkat cells as response to a 50 Hz, 0.15 mT magnetic field (MF). In contrast, a CD45-deficient Jurkat cell line was unable to respond to MF stimulation. The phosphatase activity of CD45 has been implicated to regulate p56lck tyrosine kinase activity by removing an inhibitory phosphate. By using Jurkat cells that expressed a chimeric molecule, comprising the cytoplasmic phosphatase domain of CD45, the MF induced calcium response was restored. This showed the necessity for an intact signal transduction pathway leading to a calcium increase as a result of stimulation of cells by MF. Thus, our data suggest that the target for the applied MF are molecules involved in early events in the signalling pathway from the T cell antigen receptor.

Applied weak magnetic fields have been shown to affect cellular activity on several levels, but the mechanisms involved remain elusive. We have decided to study an early signal transduction event in the human T cell line Jurkat; oscillations of free [Ca2+]i, of the type seen by crosslinking the CD3 complex. Cells were exposed to a 50 Hz, 0.1 mT, sinusoidal magnetic field while intracellular free calcium was measured in individual cells, using fura‐2 as a probe. An acute response was observed with oscillatory increases in [Ca2+]i, which subsided when the field was turned off. The effect of the magnetic field on [Ca2+]i was comparable to that achieved by an anti‐CD3 monoclonal antibody. © 1993 Wiley‐Liss, Inc.

Genomic DNA from 17 Swedish patients with familial amyloidotic polyneuropathy (FAP), and 50 healthy controls were tested with a cDNA transthyretin probe. In seven of the patients, FAP was not reported in either of their parents. All 50 controls showed restriction fragments of 6.6 kb and 3.2 kb after cleavage with Nsil, while the 17 FAP patients showed RFLP markers of 5.1 and 1.5 kb. These observations indicate the same methionine for valine substitution at position 30 in Swedish patients with FAP as seen in patients with FAP from Japan, Portugal and FAP‐patients of Swedish descent from USA. However, the mean onset of FAP symptoms for the 17 Swedish patients was found to be significantly later than for the patients from Japan, Portugal and USA.