Defective CD2 pathway T cell activation in systemic lupus erythematosus
dc.contributor.author | Fox, David A. | en_US |
dc.contributor.author | Millard, Jo Ann | en_US |
dc.contributor.author | Treisman, Jonathan | en_US |
dc.contributor.author | Zeldes, Wendy | en_US |
dc.contributor.author | Bergman, Alice | en_US |
dc.contributor.author | Depper, Joel M. | en_US |
dc.contributor.author | Dunne, Robert | en_US |
dc.contributor.author | McCune, William Joseph | en_US |
dc.date.accessioned | 2006-04-28T16:24:37Z | |
dc.date.available | 2006-04-28T16:24:37Z | |
dc.date.issued | 1991-05 | en_US |
dc.identifier.citation | Fox, David A.; Millard, Jo Ann; Treisman, Jonathan; Zeldes, Wendy; Bergman, Alice; Depper, Joel; Dunne, Robert; McCune, W. Joseph (1991)."Defective CD2 pathway T cell activation in systemic lupus erythematosus." Arthritis & Rheumatism 34(5): 561-571. <http://hdl.handle.net/2027.42/37788> | en_US |
dc.identifier.issn | 0004-3591 | en_US |
dc.identifier.issn | 1529-0131 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/37788 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1673843&dopt=citation | en_US |
dc.description.abstract | CD2 (T11; sheep erythrocyte receptor) is the surface component of an alternative, antigen-independent pathway of human T cell activation. The response to certain anti-CD2 antibodies is relatively independent of accessory cell signals and therefore provides a direct measurement of T cell function. The CD2 pathway may be important in the differentiation of thymocytes, on which the expression of CD2 precedes the appearance of the CD3–T cell receptor complex. In view of the impaired T cell regulation of immune responses in patients with systemic lupus erythematosus (SLE), we examined the activation of peripheral blood lymphocytes by anti-CD2 antibodies in 57 SLE patients and 32 normal control subjects. The CD2 pathway response was lower in the SLE patients ( P < 0.0001); 18 of the 57 SLE patients had a lower response than any of the control subjects. The SLE low-responder patients did not differ from the normal-responder patients in terms of disease activity or use of antiinflammatory and immunosuppressive medications. Low responses to anti-CD2 were corrected to normal by the coaddition of a submitogenic amount of phorbol myristate acetate (1 ng/ml). In some low-responder patients, the responses were normalized by the removal of non–T cells. The data indicate that some SLE patients have impaired responses to CD2 pathway activation and that this may reflect intrinsic T cell defects and/or regulatory influences of non–T cells. | en_US |
dc.format.extent | 1152450 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | John Wiley & Sons, Inc. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Rheumatology | en_US |
dc.title | Defective CD2 pathway T cell activation in systemic lupus erythematosus | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Geriatrics | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor ; Division of Rheumatology, R4570 Kresge Eye Institute, University of Michigan, Ann Arbor, MI 48109–0531 | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.contributor.affiliationum | Division of Rheumatology, Rackham Arthritis Research Unit, Department of Internal Medicine, and the Multipurpose Arthritis Center, University of Michigan Medical Center, Ann Arbor | en_US |
dc.identifier.pmid | 1673843 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/37788/1/1780340508_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/art.1780340508 | en_US |
dc.identifier.source | Arthritis & Rheumatism | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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