ge A Sa As perry 8 agrees aEagent be RADIATION INJURY: ITS PATHOGEN ESE AND TEREOVEY Bey conclusively proving that cellular transphentation cue apd docs take place. Lindsley cf ad. availed themselves of the blood type of certain strains of hats and proved that fametional erythropoietic tissae of the donor atid was implanted in the irradiated host and was producing cells characteristic of the donor. Ax pointed out by Ford ef af., this might be comparable to transduction in bacteria. Nowell ef af. took advantage of the fuet that rat leukocytes give a strong positive alkaline phosphatase and mouse leukecytes give a negative reaction. [rradiuted mice were injected with rat hone marrow. This increased the survival rate. Phoxphatase-positive white blood cells were found in the peripheral blood and the bone marrow showing that transplantation had in all probability occurred. Tlowever, these authors do not rule out that the phenomenon may have been indneed in the host cells; arather unlikely explanation. Ford et al. have, without doubt, proved that transplantation of donor hemopoietic cells has oecurred. They used a distinctive ‘marker chromosome” that had been induced by a radiation reciprocal translocation of chromosomes yielding a small distinctive easily detected chromosome. When spleen homogenates were prepared from the spleens of mice possessing this distinctive chromosome, the proliferative hemopoietic tissue of recipient mice consisted predominantly of the marked cells. Brocades et al. have demonstrated continued proliferation of rat lymphocytic cells in irradiated mice. Makinodan by quantitative immunological tests on red cells proved that irradiated mice heterclogously protected by rat bone marrow eventually developed 100 per cent rat red cells and also confirmed Nowell ef al. on the presence of rat granulocytes by the distinctive phosphatase reaction. It would appear that these four studies would have driveimthe last ‘‘coffin nail” into the “humoral theory of Jacobson”; however, proof of transplantation does not exchide a humoral contribution. In fact, Jaroslow and Taliaferro have apparently demon- strated that there is a noncellular factor associated with diverse mate- rials such as mouse spleen, HeLa cells, and yeast autolysate that restores the ability to produce antibodies. C. L. Miller has also demonstrated a heat labile serum factor that is necessary to retain the protective effect of cells of en.brvo spleen or liver in tissue cultures, although the fact is not necessary for viability of the culture. As indicated earlier, while protection is afforded under some cireumstances in which the injected cells are not genetically identical to those of the host. such protection is usually short-lived. Survival of the graft: and host is dependent on the histocompatibility of the antigenic pattern of the dover and host. Histoincompatibility is associated with two groups of antigens. the H-antigens that result in production of humoral antibodies, and T-antigens that produce tissue immunity but not detectable circulating antibodies. If the dose of radiation is not sufficiently high, 5012885