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Research Article Free access | 10.1172/JCI114845

Failure of T cell receptor-anti-CD3 monoclonal antibody interaction in T cells from marrow recipients to induce increases in intracellular ionized calcium.

M Yamagami, P W McFadden, S M Koethe, V Ratanatharathorn, and L G Lum

Department of Medicine, Wayne State University, Detroit, Michigan 48202.

Find articles by Yamagami, M. in: PubMed | Google Scholar

Department of Medicine, Wayne State University, Detroit, Michigan 48202.

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Department of Medicine, Wayne State University, Detroit, Michigan 48202.

Find articles by Koethe, S. in: PubMed | Google Scholar

Department of Medicine, Wayne State University, Detroit, Michigan 48202.

Find articles by Ratanatharathorn, V. in: PubMed | Google Scholar

Department of Medicine, Wayne State University, Detroit, Michigan 48202.

Find articles by Lum, L. in: PubMed | Google Scholar

Published October 1, 1990 - More info

Published in Volume 86, Issue 4 on October 1, 1990
J Clin Invest. 1990;86(4):1347–1351. https://doi.org/10.1172/JCI114845.
© 1990 The American Society for Clinical Investigation
Published October 1, 1990 - Version history
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Abstract

There are multiple immune defects in T cells from recipients after bone marrow transplantation (BMT). This study examines recipient T cells for increases in intracellular ionized calcium concentration [( Ca2+]i) after binding the T cell receptor-CD3 complex with anti-CD3 MAb. PBL from 10 of 23 short-term recipients (less than 1 yr after BMT) responded poorly (less than 35% of control) to anti-CD3 stimulation and PBL from 9 of 23 had blunted calcium flux responses (35-70% of control). Purified CD2+, CD56- cells from seven additional short-term recipients including three autologous marrow recipients were closely examined, and a sizable proportion of CD3+ cells from six of seven recipients did not increase [Ca2+]i after anti-CD3 stimulation. The decreased magnitude of the responses was due to decreased numbers of responding cells and not to a decrease in mean CD3 fluorescent intensity or in calcium flux responses on a single cell basis. Five of seven long-term recipients (greater than 1 yr after BMT) had PBL that responded normally and two of seven had PBL with blunted calcium flux responses. The data show that the signal transduction response mediated by the CD3-antigen receptor as measured by calcium flux is defective early after autologus or allogeneic BMT.

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