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PubMed1983

[Lack of relationship between viral leukemogenesis and immunosuppression in the mouse].

The relationship between immunodepression and leukemogenesis induced by a murine retro-virus. PLLV-T2, was studied in different strains of mice. Cellular immunity, using as parameters both allograft rejection and graft versus host reaction, was not affected during the early phase of leukemia development. As for humoral immunity, determined by the response to xenogeneic red blood cells and to lipopolysaccharides, no direct relationship between the immunodepression caused by the retrovirus and leukemogenesis could be encountered: in certain strains, such as DBA/2, with susceptibility to leukemogenesis similar to that of BALB/c, no decrease in the immune response was registered during the early phase of the disease. The results obtained demonstrate that immunodepression is not a necessary condition for the clinical appearance of this viral-induced leukemia indicating that humoral and/or cellular immunity would not play an important role as surveillance mechanism against this neoplasia.

Animals↗
PubMed1983

The asymmetry in idiotype-isotype expression in the response to phosphocholine is due to divergence in the expressed repertoires of Lyb-5+ and Lyb-5- B cells.

The X-linked CBA/N immune defect was used to investigate the roles of Lyb-5- and Lyb-5+ B cells in the memory response to PC-KLH (phosphocholine-conjugated keyhole limpet hemocyanin). (CBA/N X BALB/c)F1 (CB) male mice express the xid mutation and thereby lack the Lyb-5+ B cell subset, whereas their female littermates are normal and express both Lyb-5+ and Lyb-5- B cells. After priming with PC-conjugated hemocyanin (PC-Hy) in complete Freund's adjuvant, female B cells produce three phenotypic sets of PC-KLH-specific antibody. The first set (group I) is dominated by T15+, IgM, IgA, and IgG3, PC-specific antibodies. The second subset (group II) is specific for phenylphosphocholine (PPC), and is dominated by T15-, IgG1, and IgG2 antibodies. The third set (group III) recognizes an epitope(s) composed of both the PPC hapten and carrier determinants. PC-Hy-primed B cells from immune defective CB male mice produce the same number of IgG1 and IgG2 plaque-forming cells (PFC) as do PC-Hy-primed normal female cells, and these PFC are also predominantly T15- and PPC specific (group II). In addition, a significant amount of group III IgG1 and IgG2 antibody is observed in the immune defective male response. In contrast to female B cells, immune defective male B cells produce a low IgM, IgA, and IgG3 memory response that is not composed of PC-specific (group I) antibodies; in fact, most of these antibodies arise from group III precursors and are not inhibited by either PC or PPC. PC-specific antibodies usually represent less than 25% of the anti-PC-KLH response in immune defective mice; however, these PC-specific antibodies are predominantly T15-. These data suggest that the Lyb-5-B cells in both normal and immune defective mice produce the T15-, IgG1, and IgG2 antibodies that dominate the secondary immune response to PC-KLH, and that the Lyb-5+ B cells produce the T15+, IgM, IgA, and IgG3 portion of the secondary response in normal mice. This hypothesis was confirmed by priming normal mice with the R36a strain of Streptococcus pneumoniae or with PC-Hy in saline. These forms of PC-antigen prime only the Lyb-5+ B cell subset. The adoptive transfer of these two B cell sources results in an anti-PC-KLH response that is T15 dominant and totally PC inhibitable.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

[Cancer and immunosuppression : experimental aspects].

The hypothesis that immunodepression favors a carcinogenetic process and thus subsequent tumor development remains controversial in spite of numerous experimental studies. This is due, on one hand, to the difficulty in demonstrating the presence of tumor-associated antigens and, on the other, to the complex immunological mechanisms which lead to the destruction of tumors cells. With respect to immunosurveillance, the present situation can be summarized as follows: the development of virus-induced tumors is under the control of a T-cell dependent system; a T-cell depression (thymectomy, congenital absence of thymus, anti-lymphocytic serum) increases the number of these tumors; chemically induced tumors or spontaneous tumors are under the control of non-specific effectors such as macrophages and NK cells; NK cell deficiency (of congenital origin such as in beige mice) or acquired (chemically induced) increases tumor growth; carcinogens can induce general immunodepression (chemical carcinogenesis) or stimulate specific suppressive cells (U.V. radiation) thus allowing tumors development. The tumors being established, it may itself contribute to an immunodepressive state thus fostering its growth through the activity of: immune complexes; specific or non specific suppressive cells; an increase in the level of alpha 2-globulin immunosuppressive molecules which are present under normal conditions; a release of several factors acting at different levels such as prostaglandin E, anti-inflammatory factors acting on monocytes, etc. The apparition of an antigenic and immunogenic tumor heterogeneity due to development of new clones will also modify host-tumor relationships. The complexity of the immunological mechanisms which are involved in the control of tumor growth may explain the variable results of immune prevention and of the immunotherapy of cancer.

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