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J M Depper

Publications and source records attributed to J M Depper.

40 records · Page 3Linked to original sources
PubMed1981

Impaired regulation of Epstein-Barr virus-induced lymphocyte proliferation in rheumatoid arthritis is due to a T cell defect.

The rate of outgrowth of EBV-infected B lymphocytes is regulated by normal T lymphocytes. Removal of T cells from normal whole lymphoid populations (PBM) markedly shortens the outgrowth time of the remaining B lymphocytes. There is little difference in the much more rapid outgrowth of rheumatoid PBM after the removal of T cells, which suggests that RA lymphoid cells are unable to regulate this process. To determine whether RA T cells are defective, or EBV-infected RA B cells are unresponsive to regulatory signals, EBV-induced outgrowth in autologous and allogeneic mixtures of RA and normal B and T cells was evaluated, employing morphologic criteria and 3H-thymidine incorporation. The difference in outgrowth between RA and normal PBM was reproduced by reconstitution of EBV-infected B cells with mitomycin-treated autologous T cells. In cell-mixing experiments, normal T cells appropriately regulated both normal and RA B cells similarly, whereas RA T cells were defective in regulating either B cell population. Thus, the rapid outgrowth of EBV-infected rheumatoid lymphoid cells is due to defective T cell regulation. Moreover, normal regulation does not require cell proliferation.

Antibodies, Viral↗
PubMedDate not supplied

Molecular cloning and expression of cDNAs for the human interleukin-2 receptor.

We have purified the human T-cell growth factor (interleukin-2) receptor and have cloned, sequenced and expressed cDNAs corresponding to this receptor. We identify one gene, but two interleukin-2 receptor mRNAs which differ in their polyadenylation signals. We have isolated an additional cDNA that may correspond to an alternatively spliced mRNA that lacks a 216 base segment and appears to encode an altered membrane protein which cannot bind interleukin-2.

Amino Acid Sequence↗