TY - JOUR
T1 - Nonencephalitogenic CD4-CD8- Vα2Vβ8.2+ anti-myelin basic protein rat T lymphocytes inhibit disease induction
AU - Lider, Ofer
AU - Miller, Ariel
AU - Miron, Shmuel
AU - Hershkoviz, Rami
AU - Weiner, Howard L.
AU - Zhang, Xiangming
AU - Heber-Katz, Ellen
PY - 1991/8/15
Y1 - 1991/8/15
N2 - Recently there has been a number of reports suggesting that CD4-CD8- T cells participate in the processes of inflammatory reaction. In an attempt to delineate the distinctive functions of double negative (DN) T lymphocytes in an autoimmune-induced disease, we isolated and cloned such T cells, along with control CD4+ cells, from Lewis rats immunized with guinea-pig myelin basic protein in CFA. Both clones proliferated in response to the guinea-pig myelin basic protein and its synthetic encephalitogenic peptide, and expressed the same TCR V genes homologous to the mouse Vα2 and Vβ8.2 families that appear to be the defining entity of experimental autoimmune encephalomyelitis (EAE). Moreover, the TCR D and J region gene products of the DN cell were found to be similar to another encephalitogenic rat T cell clone. The two T clones did not differ markedly in their ability to produce TNF and IL-2 and to adhere to vascular wall-derived extracellular matrix- and laminin-coated plates. Surprising, therefore, was the finding that, although the CD4+ T lymphocytes were capable of inducing EAE, the DN cells did not elicit disease but rather inhibited subsequent EAE induction. Thus, TCR Vα2V/β8.2 and its junctional region gene products are not the only prerequisite segment for a T cell to become encephalitogenic. We suggest that the important determinants of the T cell ability to induce disease are features of the T cell, other than or in addition to, the T cell receptor.
AB - Recently there has been a number of reports suggesting that CD4-CD8- T cells participate in the processes of inflammatory reaction. In an attempt to delineate the distinctive functions of double negative (DN) T lymphocytes in an autoimmune-induced disease, we isolated and cloned such T cells, along with control CD4+ cells, from Lewis rats immunized with guinea-pig myelin basic protein in CFA. Both clones proliferated in response to the guinea-pig myelin basic protein and its synthetic encephalitogenic peptide, and expressed the same TCR V genes homologous to the mouse Vα2 and Vβ8.2 families that appear to be the defining entity of experimental autoimmune encephalomyelitis (EAE). Moreover, the TCR D and J region gene products of the DN cell were found to be similar to another encephalitogenic rat T cell clone. The two T clones did not differ markedly in their ability to produce TNF and IL-2 and to adhere to vascular wall-derived extracellular matrix- and laminin-coated plates. Surprising, therefore, was the finding that, although the CD4+ T lymphocytes were capable of inducing EAE, the DN cells did not elicit disease but rather inhibited subsequent EAE induction. Thus, TCR Vα2V/β8.2 and its junctional region gene products are not the only prerequisite segment for a T cell to become encephalitogenic. We suggest that the important determinants of the T cell ability to induce disease are features of the T cell, other than or in addition to, the T cell receptor.
UR - http://www.scopus.com/inward/record.url?scp=0025789087&partnerID=8YFLogxK
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C2 - 1714476
AN - SCOPUS:0025789087
SN - 0022-1767
VL - 147
SP - 1208
EP - 1213
JO - Journal of Immunology
JF - Journal of Immunology
IS - 4
ER -