Abstract
The generation of an in vitro major histocompatibility complex class I specifie response of CD4-CD8- T cell receptor (TCR) αβ cytotoxic T lymphocytes (CTL) and their allogeneic tumor rejection were investigated. Inocula of BALBRL♂ 1 were rejected in C57BL/6 (B6) mice treated with minimum essential medium (MEM) (control), anti-L3T4 (CD4) monoclonal antibody (mAb) or anti-Lyt-2.2 (CD8) mAb and CTL against the tumor were generated in vitro. No rejection and no induction of CTL were observed in B6 mice treated with anti-L3T4 (CD4) plus anti-Lyt-2.2 (CD8) mAb. CTL with the classical Thy-1+CD3+CD4-CD8+ TCR αβ phenotype were generated in mixed lymphocyte tumor cell culture (MLTC) spleen cells from B6 mice treated with MEM (control) or anti-L3T4 (CD4) mAb, whereas CTL with an unusual Thy-1+ CD3+ CD4-CD8- TCR αβ phenotype were generated in MLTC spleen cells from anti-Lyt-2.2 (CD8) mAb-treated B6 mice. Both types of CTL were reactive with both H-2Kd and Dd (Ld) class I antigen. These findings suggest that when CD4+ cells were blocked by antiL3T4 (CD4) mAb, CD8+ CTL mediated rejection, and when CD8+ cells were blocked by anti-Lyt-2.2 (CD8) mAb, CD4+ cells were capable of mediating rejection, although less efficiently than CD8+ cells, by inducing CD4-CD8+ TCR αβ CTL. The finding that adoptive transfer of CD4 and CD8-depleted MLTC spleen cells, obtained from anti-Lyt-2.2 (CD8) mAbtreated B6 mice that had rejected BALBRL♂ 1, resulted in rejection of BALBRL♂ 1 inoculated into B6 nu/nu mice confirmed the above notion. CTL clones with the CD4-CD8- TCR αβ phenotype specific for Ld were established.
| Original language | English |
|---|---|
| Pages (from-to) | 193-201 |
| Number of pages | 9 |
| Journal | Journal of Experimental Medicine |
| Volume | 174 |
| Issue number | 1 |
| Publication status | Published - 1991 |
| Externally published | Yes |
Fingerprint
ASJC Scopus subject areas
- Immunology
Cite this
CD4-CD8- T cell receptor αβ T cells : Generation of an in vitro major histocompatability complex class I specific cytotoxic T lymphocyte response and allogeneic tumor rejection. / Mieno, Masahiro; Suto, Ryuichiro; Obata, Yuichi; Udono, Heiichiro; Takahashi, Toshitada; Shiku, Hiroshi; Nakayama, Eiichi.
In: Journal of Experimental Medicine, Vol. 174, No. 1, 1991, p. 193-201.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - CD4-CD8- T cell receptor αβ T cells
T2 - Generation of an in vitro major histocompatability complex class I specific cytotoxic T lymphocyte response and allogeneic tumor rejection
AU - Mieno, Masahiro
AU - Suto, Ryuichiro
AU - Obata, Yuichi
AU - Udono, Heiichiro
AU - Takahashi, Toshitada
AU - Shiku, Hiroshi
AU - Nakayama, Eiichi
PY - 1991
Y1 - 1991
N2 - The generation of an in vitro major histocompatibility complex class I specifie response of CD4-CD8- T cell receptor (TCR) αβ cytotoxic T lymphocytes (CTL) and their allogeneic tumor rejection were investigated. Inocula of BALBRL♂ 1 were rejected in C57BL/6 (B6) mice treated with minimum essential medium (MEM) (control), anti-L3T4 (CD4) monoclonal antibody (mAb) or anti-Lyt-2.2 (CD8) mAb and CTL against the tumor were generated in vitro. No rejection and no induction of CTL were observed in B6 mice treated with anti-L3T4 (CD4) plus anti-Lyt-2.2 (CD8) mAb. CTL with the classical Thy-1+CD3+CD4-CD8+ TCR αβ phenotype were generated in mixed lymphocyte tumor cell culture (MLTC) spleen cells from B6 mice treated with MEM (control) or anti-L3T4 (CD4) mAb, whereas CTL with an unusual Thy-1+ CD3+ CD4-CD8- TCR αβ phenotype were generated in MLTC spleen cells from anti-Lyt-2.2 (CD8) mAb-treated B6 mice. Both types of CTL were reactive with both H-2Kd and Dd (Ld) class I antigen. These findings suggest that when CD4+ cells were blocked by antiL3T4 (CD4) mAb, CD8+ CTL mediated rejection, and when CD8+ cells were blocked by anti-Lyt-2.2 (CD8) mAb, CD4+ cells were capable of mediating rejection, although less efficiently than CD8+ cells, by inducing CD4-CD8+ TCR αβ CTL. The finding that adoptive transfer of CD4 and CD8-depleted MLTC spleen cells, obtained from anti-Lyt-2.2 (CD8) mAbtreated B6 mice that had rejected BALBRL♂ 1, resulted in rejection of BALBRL♂ 1 inoculated into B6 nu/nu mice confirmed the above notion. CTL clones with the CD4-CD8- TCR αβ phenotype specific for Ld were established.
AB - The generation of an in vitro major histocompatibility complex class I specifie response of CD4-CD8- T cell receptor (TCR) αβ cytotoxic T lymphocytes (CTL) and their allogeneic tumor rejection were investigated. Inocula of BALBRL♂ 1 were rejected in C57BL/6 (B6) mice treated with minimum essential medium (MEM) (control), anti-L3T4 (CD4) monoclonal antibody (mAb) or anti-Lyt-2.2 (CD8) mAb and CTL against the tumor were generated in vitro. No rejection and no induction of CTL were observed in B6 mice treated with anti-L3T4 (CD4) plus anti-Lyt-2.2 (CD8) mAb. CTL with the classical Thy-1+CD3+CD4-CD8+ TCR αβ phenotype were generated in mixed lymphocyte tumor cell culture (MLTC) spleen cells from B6 mice treated with MEM (control) or anti-L3T4 (CD4) mAb, whereas CTL with an unusual Thy-1+ CD3+ CD4-CD8- TCR αβ phenotype were generated in MLTC spleen cells from anti-Lyt-2.2 (CD8) mAb-treated B6 mice. Both types of CTL were reactive with both H-2Kd and Dd (Ld) class I antigen. These findings suggest that when CD4+ cells were blocked by antiL3T4 (CD4) mAb, CD8+ CTL mediated rejection, and when CD8+ cells were blocked by anti-Lyt-2.2 (CD8) mAb, CD4+ cells were capable of mediating rejection, although less efficiently than CD8+ cells, by inducing CD4-CD8+ TCR αβ CTL. The finding that adoptive transfer of CD4 and CD8-depleted MLTC spleen cells, obtained from anti-Lyt-2.2 (CD8) mAbtreated B6 mice that had rejected BALBRL♂ 1, resulted in rejection of BALBRL♂ 1 inoculated into B6 nu/nu mice confirmed the above notion. CTL clones with the CD4-CD8- TCR αβ phenotype specific for Ld were established.
UR - http://www.scopus.com/inward/record.url?scp=0025822209&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025822209&partnerID=8YFLogxK
M3 - Article
C2 - 1905338
AN - SCOPUS:0025822209
VL - 174
SP - 193
EP - 201
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
SN - 0022-1007
IS - 1
ER -