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[Cancer Research 33, 2247-2256, October 1, 1973]
© 1973 American Association for Cancer Research

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The Stimulatory Effect of Tumor Bearing upon the T- and B-Cell Subpopulations of the Mouse Spleen1

Susumu Konda, Yoshinobu Nakao and Richard T. Smith

The Tumor Biology Unit, Department of Pathology, College of Medicine, University of Florida, Gainesville, Florida 32601

The numbers and certain functions of T- and B-cell subpopulations of the spleen have been assessed in C57BL/6 and CBA mice over the course of bearing transplanted, syngeneic methylcholanthrene fibrosarcomas. The level of proliferative activity in this population increases progressively over the 5- to 8-week course of tumor bearing. The size of the {theta}-antigen-bearing subpopulation and the T-cell functions of graft-versus-host reactivity, in vitro responses to phytohemagglutinin, and primary stimulation by alloantigen in one-way mixed leukocyte cultures were found to increase significantly, provided that the data are expressed on the basis of total numbers of cells or degree of total function in the spleen. Numbers of plaque- or rosette-forming cells per spleen also increased over control values, both after direct immunization with sheep erythrocytes and when the primary response of spleen cells to sheep red blood cells was assayed adoptively in an irradiated host. The subpopulation responding to the mitogenic effect of lipopolysaccharide in vitro was greatly increased during tumor bearing. The data suggest that both T- and B-cell subpopulations and their functions are not diminished but are augmented significantly by tumor bearing.

1 This paper was supported in part by grants from the American Cancer Society (a Henry J. Leonard Memorial Grant for Cancer Research, ACS-ET-6B), the Florida Division of the American Cancer Society (F-7-OUF), and the National Institute of Child Health and Human Development (HD-00384); an American Cancer Society Institutional Grant (IN-62-G), and training grants from the National Institute of General Medical Sciences (GM-01996) and the National Institute of Allergy and Infectious Diseases (AI-00401).

Received 3/23/73. Accepted 6/ 8/73.







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Copyright © 1973 by the American Association for Cancer Research.