Suppression of lymphocyte spontaneous proliferative response by proteolipid protein peptide in patients with HAM/TSP |
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Authors: | Takeshi Tabira Jun-ichi Inobe Keiichi Nakahara Mitsuhiro Osame Takashi Yamamura |
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Affiliation: | (1) Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, 4-1-1 Ogawa-higashi, 187 Kodaira, Tokyo, Japan;(2) The Third Department of Internal Medicine, Kagoshima University, Kagoshima, Japan |
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Abstract: | To understand the immune mechanism suggested in HTLV-I-associated myelopathy (HAM/TSP), we investigated T cell response to proteolipid protein (PLP). Because of high autologous proliferative response (APR) of peripheral blood mononuclear cells (PBMC) in culture, the lymphocyte proliferation assay was not useful in this disease. Unexpectedly, however, APR was profoundly (70–98%) suppressed in 6 of 9 cases when PLP peptide 105-124 was added in the culture. PLP peptide 85-104 or 145-159 also suppressed APR in a few cases. Time course study showed that the peptide-mediated suppression became apparent after day 4 in culture. The results can be interpreted as that suppressor cells recognizing the PLP peptides were present in the PBMC of HAM/TSP patients and suppressed the APR as the consequence of antigen specific response. This may indicate that a T cell response to certain PLP determinants is involved in the pathomechanism of HAM/TSP at least in part. Molecular mimicry between PLP and HTLV-I mayaccount for the T cell sensitization to PLP in HAM/TSP.Special issue dedicated to Dr. Marjorie B. Lees. |
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Keywords: | Proteolipid protein HAM/TSP T cell myelin HTLV-I |
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