HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wakamatsu, S.-i. Articles by Baba, M. Search for Related Content PubMed PubMed Citation Articles by Wakamatsu, S.-i. Articles by Baba, M.

Monocyte-Driven Activation-Induced Apoptotic Cell Death of Human T-Lymphotropic Virus Type I-Infected T Cells¹

Shin-ichi Wakamatsu^*,, Masahiko Makino^2,*, Chuuwa Tei and Masanori Baba^*

^* Division of Human Retroviruses, Center for Chronic Viral Diseases, and First Internal Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan

We attempted apoptotic cell death induction of T cells infected with human T lymphotropic virus type I (HTLV-I) which induces HTLV-I-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia. T cells acutely infected and expressing HTLV-Igag Ags were killed by cross-linking their TCR with anti-CD3 mAb. Cells in apoptotic process were found by staining with annexin V. The apoptosis was not affected by costimulation through CD28 molecules and was resistant to ligation of Fas molecules. Whereas the virus-infected T cells expressed higher levels of HLA-DR, CD25, CD80, and CD86 Ags than apoptosis-resistant PHA-blasts, the T cell apoptosis was enhanced by addition of exogenous IL-2. Furthermore, in this apoptosis, monocytes played an important role because T cells infected in the absence of monocytes were resistant to the death signals. The apoptosis-sensitive T cells responded to TCR signaling more strongly by proliferating than those apoptosis-resistant cells. Monocytes weakly affected the expression levels of viral Ags on T cells. However, HTLV-I-infected monocytes primed T cells to die by subsequent TCR signaling. T cells primed with the monocytes, subsequently infected in the absence of monocytes, were killed by TCR signaling. These observations suggest that primed and infected T cells could be killed by activation-induced cell death.

This article has been cited by other articles:

				M. Makino, Y. Maeda, and K. Inagaki Immunostimulatory Activity of Recombinant Mycobacterium bovis BCG That Secretes Major Membrane Protein II of Mycobacterium leprae. Infect. Immun., November 1, 2006; 74(11): 6264 - 6271. [Abstract] [Full Text] [PDF]

				Y. Maeda, T. Mukai, J. Spencer, and M. Makino Identification of an Immunomodulating Agent from Mycobacterium leprae Infect. Immun., May 1, 2005; 73(5): 2744 - 2750. [Abstract] [Full Text] [PDF]