Treatment of a low immunogenic experimental tumour with alloactivated or tumour-immune lymphocytes

1987 ◽  
Vol 907 (2) ◽  
pp. 163-174 ◽  
Author(s):  
Giorgio Parmiani ◽  
Laura Grazioli ◽  
Marialuisa Sensi ◽  
Mario P. Colombo ◽  
Monica Rodolfo
1975 ◽  
Vol 141 (1) ◽  
pp. 11-26 ◽  
Author(s):  
B D Brondz ◽  
I K Egorov ◽  
G I Drizlikh

Receptors of effector T lymphocytes of congeneic strains of mice do not recognize public H-2 specificities and react to private H-2 specificities only. This has been established with the use of three tests: direct cytotoxicity assay of immune lymphocytes upon target cells, specific absorption of the lymphocytes on the target cells, and rejection of skin grafts at an accelerated fashion. Immunization with two private H-2 specificities in the system C57BL/10ScSn leads to B10.D2 induces formation of two corresponding populations of effector lymphocytes in unequal proportion: a greater part of them is directed against the private specificity H-2.33 (Kb), while the smaller part is towards H-2.2 (Db) private specificity. These two populations of effector lymphocytes do not overlap, as demonstrated by experiments on their cross-absorption on B10.D2 (R107), B10.D2 (R101), B10.A(2R), and B10.A(5R) target cells, as well as on mixtures of R107 and R101 targets. Following removal of lymphocytes reacting with one of the private H-2 specificities, lymphocytes specific to the other specificity are fully maintained. A mixture of target cells, each bearing one of the two immunizing private specificities, absorbs 100% of the immune lymphocytes and is totally destroyed by them. It is suggested that H-2 antigens are natural complexes of hapten-carrier type, in which the role of hapten is played by public H-2 specifities and that of the carrier determinant by either private H-2 specificities or structures closely linked to them. Various models of steric arrangement of MHC determinants recognized by receptors of effector T lymphocytes are discussed.


1976 ◽  
Vol 144 (3) ◽  
pp. 776-787 ◽  
Author(s):  
R M Zinkernagel

In mice, primary footpad swelling after local infection with lymphocytic choriomeningitis virus (LCMV) and delayed-type hypersensitivity (DTH) adoptively transferred by LCMV immune lymphocytes are T-cell dependent. Nude mice do not develop primary footpad swelling, and T-cell depletion abrogates the capacity to transfer LCMV-specific DTH. Effector T cells involved in eliciting dose-dependent DTH are virus specific in that vaccinia virus-immune lymphocytes could not elicit DTH in LCMV-infected mice. The adoptive transfer of DTH is restricted to H-2K or H-2D compatible donor-recipient combinations. Distinct from the fowl-gamma-globulin DTH model, I-region compatibility is neither necessary nor alone sufficient. Whatever the mechanisms involved in this K- or D-region associated restriction in vivo, it most likely operates at the level of T-cell recognition of "altered self" coded in K or D. T cells associated with the I region (helper T cells and DTH-T cells to fowl-gamma-globulin) are specific for soluble, defined, and inert antigens. T cells associated with the K and D region (T cells cytotoxic in vitro and in vivo for acute LCMV-infected cells, DTH effector T cells, and anti-viral T cells) are specific for infectious, multiplying virus. The fact that T-cell specificity is differentially linked with the I region or with the K and D regions of H-2 may reflect the fundamental biological differences of these antigens. Although it cannot be excluded that separate functional subclasses of T-effector cells could have self-recognizers for different cell surface structures coded in I or K and D, it is more likely that the antigen parameters determine whether T cells are specific for "altered" I or "altered" K- or D-coded structures.


1981 ◽  
Vol 4 (4) ◽  
pp. 185-190 ◽  
Author(s):  
Y. Matsuoka ◽  
K. -A. Hossmann

1994 ◽  
Vol 8 (3) ◽  
pp. 218-223 ◽  
Author(s):  
Shinichiro Yasumoto ◽  
Yoichi Moroi ◽  
Tetsuya Koga ◽  
Ikuo Kawamura ◽  
Masao Mitsuyama ◽  
...  

1994 ◽  
Vol 41 (1) ◽  
pp. 13-16
Author(s):  
J Batko ◽  
H Karoń

Changes in the content of N-acetylneuraminic acid in rat erythrocyte membranes at different stages of experimental tumour (Morris hepatoma 5123) development were examined. Its content was lowered on the 30th and 40th day after transplantation of the tumour cells, as compared to the results for normal healthy rats. As a result of the tumour growth, the content of N-acetylgalactosamine, galactose and mannose in rat erythrocyte membranes became lowered, whereas that of glucose remained unchanged. The content of fucose was raised at early stage of tumour growth, and remained at this high level till the 40th day of experiment.


1977 ◽  
Vol 1 (2) ◽  
pp. 123-135 ◽  
Author(s):  
G BULLOCK ◽  
M JASANI ◽  
G LEWIS
Keyword(s):  

1962 ◽  
Vol 115 (3) ◽  
pp. 475-489 ◽  
Author(s):  
Jacob Fong ◽  
Dennis Chin ◽  
Sanford S. Elberg

Studies of passive transfer of cellular resistance, as manifested by refractoriness to necrotization with virulent tubercle bacilli, have shown that immune histiocytes or immune lymphocytes were effective transferring agents; immune polymorphonuclear leucocytes and immune serum as well as comparable cells from normal animals lacked this capacity. Comparisons of immune histiocytes and immune lymphocytes showed that the former cells were more efficient; this was indicated by (a) the smaller numbers of immune histiocytes needed for passive transfer, (b) the longer duration of cellular resistance in recipients given histiocytes than in those given lymphocytes, (c) the greater capacity of histiocytes to effect serial passive transfer, and (d) the ability of histiocytic but not lymphocytic lysates to transfer cellular resistance. Experiments to establish the mechanism of passive transfer of cellular resistance showed that there was no active induction of resistance in recipients through transfer of bacillary antigens contained in immune histiocytes; in fact, the results of serial passive transfers with immune histiocytes suggested an active replication of the "cell resistance factor."


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