Autologous tumour-specific cytotoxic T-cell clone established from tumour-infiltrating lymphocytes (TIL) of malignant ascites in the absence of recombinant interleukin 2(rIL2): Activation by autologous tumour cell alone

Biotherapy ◽  
1993 ◽  
Vol 6 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Mitsuo Katano ◽  
Fumio Nagumo ◽  
Eiro Kubota ◽  
Hiroshi Yamamoto ◽  
Tatsuya Matsuo ◽  
...  
1983 ◽  
Vol 157 (2) ◽  
pp. 705-719 ◽  
Author(s):  
S C Meuer ◽  
K A Fitzgerald ◽  
R E Hussey ◽  
J C Hodgdon ◽  
S F Schlossman ◽  
...  

Monoclonal antibodies were produced against a human cytotoxic T cell clone, CT8III (specificity: HLA-A3), with the view of defining clonally restricted (clonotypic) surface molecules involved in its antigen recognition function. Two individual antibodies, termed anti-Ti1A and anti-Ti1B, reacted exclusively with the CT8III clone when tested on a panel of 80 additional clones from the same donor, resting or activated T cells, B cells, macrophages, thymocytes, or other hematopoietic cells. More importantly, the two antibodies inhibited cell-mediated killing and antigen-specific proliferation of the CT8III clone but did not affect the functions of any other clone tested. This inhibition was not secondary to generalized abrogation of the CT8III clone's function, because interleukin 2 responsiveness was enhanced. To examine the relationship of the structures defined by anti-clonotypic antibodies with known T cell surface molecules, antibody-induced modulation studies and competitive binding assays were performed. The results indicated that the clonotypic structures were associated with, but distinct from, the 20,000-mol wt T3 molecule expressed on all mature T lymphocytes. Moreover, in contrast to anti-T3, anti-Ti1A and anti-Ti1B each immunoprecipitated two molecules of 49,000 and 43,000-mol wt from 131I-labeled CT8III cells under reducing conditions. The development of monoclonal antibodies to such polymorphic T cell surface structures should provide important probes to further define the surface receptor for antigen.


Blood ◽  
2005 ◽  
Vol 106 (8) ◽  
pp. 2769-2780 ◽  
Author(s):  
Marcin W. Wlodarski ◽  
Christine O'Keefe ◽  
Evan C. Howe ◽  
Antonio M. Risitano ◽  
Alexander Rodriguez ◽  
...  

AbstractT-cell large granular lymphocyte (T-LGL) leukemia is a clonal lymphoproliferation of cytotoxic T cells (CTLs) associated with cytopenias. T-LGL proliferation seems to be triggered/sustained by antigenic drive; it is likely that hematopoietic progenitors are the targets in this process. The antigen-specific portion of the T-cell receptor (TCR), the variable beta (VB)–chain complementarity-determining region 3 (CDR3), can serve as a molecular signature (clonotype) of a T-cell clone. We hypothesized that clonal CTL proliferation develops not randomly but in the context of an autoimmune response. We identified the clonotypic sequence of T-LGL clones in 60 patients, including 56 with known T-LGL and 4 with unspecified neutropenia. Our method also allowed for the measurement of clonal frequencies; a decrease in or loss of the pathogenic clonotype and restoration of the TCR repertoire was found after hematologic remission. We identified 2 patients with identical immunodominant CDR3 sequence. Moreover, we found similarity between multiple immunodominant clonotypes and codominant as well as a nonexpanded, “supporting” clonotypes. The data suggest a nonrandom clonal selection in T-LGL, possibly driven by a common antigen. In contrast, the physiologic clonal CTL repertoire is highly diverse and we were not able to detect any significant clonal sharing in 26 healthy controls.


1993 ◽  
Vol 68 (3) ◽  
pp. 256-262 ◽  
Author(s):  
Takashi Okino ◽  
Nitya G. Chakraborty ◽  
Paul Stabach ◽  
Daniel R. Twardzik ◽  
Steven J. Padula ◽  
...  

Immunology ◽  
2001 ◽  
Vol 102 (1) ◽  
pp. 8-14 ◽  
Author(s):  
T. Preckel ◽  
S Hellwig ◽  
U Pflugfelder ◽  
M. B. Lappin ◽  
H. U. Weltzien

1992 ◽  
Vol 154 (2) ◽  
pp. 235-243 ◽  
Author(s):  
Yoshimasa Wada ◽  
Hideyuki Ikeda ◽  
Daisuke Ueda ◽  
Masahiko Ohta ◽  
Shuji Takahashi ◽  
...  

Virology ◽  
1987 ◽  
Vol 160 (1) ◽  
pp. 278-280 ◽  
Author(s):  
Judy M. Bastin ◽  
Alain R.M. Townsend ◽  
Andrew J. McMichael

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