TY - JOUR
T1 - Nonencephalitogenic CD4-CD8- Vα2Vβ8.2+ anti-myelin basic protein rat T lymphocytes inhibit disease induction
AU - Lider, O.
AU - Miller, A.
AU - Miron, S.
AU - Hershkoviz, R.
AU - Weiner, H. L.
AU - Zhang, X.
AU - Heber-Katz, E.
PY - 1991
Y1 - 1991
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 Vα2Vβ8.2 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 Vα2Vβ8.2 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
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
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 -