Slavin et al. in [1976], were the first to found that rejection of skin and heart allograft was greatly delayed in rodents treated with Total Lymphoid Irradiation (TLI). Since 1980, the immunosupression of TLI has been applied in transplants and autoimmune diseases. However, the development of immunosuppressive drugs decreased the use of radiotherapy for immunosuppressive finality except for the use of total body irradiation (TBI) or TLI as myeloablative treatment before bone marrow transplantation The mechanism by which TLI-treated patients have a graft prolongation is not entirely understood. During many years of its use many changes has been observed specially in lymphocytes counts. The majority of the studies, however, were done without modern techniques to characterize the fate of different subtypes of lymphocytes and is difficult to compare the results. The majority of the studies has been done in vitro and in regimes using TBI and bone marrow transplants. There is some evidence that suppressor T-cells might be involved in the long term maintenance of allografts in these patients [Gray et al, 1989]. TLI provokes a more pronounced impairment of T-dependent immunological functions, as measured with phytohemaglutinin(PHA), concanavalin A(Con A), and pokeveedinduced (PWM) blastogenesis than does conventional immunosuppression. The more profound changes in the balance between T helper and T suppressor cells after TLI are also associated with a more pronounced suppressor cell activity, as measured with different functional suppressor cell assays. [Fergunson et al, 1981; Waer et al, 1987]. The TLI seems to produce an “amnesic state” and the autoantigens cannot be recognized by the host anymore. In the past, radiation therapy had traditionally been viewed as immunosuppressive (Cole, 1986; James et al., 1989; Wasserman et al., 1989). Lymphocyte radiosensitivity is well established and remains the dominant explanation for this effect. However, substantial evidence suggests more varied effects of radiation on the immune system, prompting the recharacterization of radiation as ‘immunomodulatory’ rather than immunosuppressive (McBride et al., 2004). Ionising radiation induces diverse effects on cell survival, apoptosis, proliferation and differentiation depending on the dosage and target cell (Jonathan et al. 1999). High dose of radiation often results in massive DNA damage that involves double-strand breaks and subsequent cell death. Low dose of irradiation induces reactive oxygen species (ROS) and the activation of specific intracellular signaling pathways and transcription factors leading to proliferation and differentiation of target cells (Kasid et al. 1996, Lander et al. 1997, Finkel 1998). Therefore, irradiation can modulate immune response via its variable effects on immune cell survival and differentiation (Shankar et al. 1999, Rho et al. 2004, Liu 2007, Shan et al.2007).
ABSTRACT
PUBLICATION RECORD
- Publication year
2012
- Venue
Unknown venue
- Publication date
2012-02-24
- Fields of study
Medicine, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar
CITATION MAP
EXTRACTION MAP
CLAIMS
- No claims are published for this paper.
CONCEPTS
- No concepts are published for this paper.
REFERENCES
CITED BY
Showing 1-1 of 1 citing papers · Page 1 of 1