Post-infection genetic resistance to avian lymphoid leukosis resides in B target cell

Abstract

NEOPLASMS in which the target for transformation is a B-dependent lymphoid cell include Burkitt's lymphoma¹ and chronic lymphocytic leukaemia² of man, bovine leukaemia³ and lymphoid leukosis in chickens^4–11. Inherited resistance to the development of tumours may involve at the first level, a resistance of all cells in the body to infection by tumour viruses or, at the second level, a failure of the tumour to develop or progress in virus-infected animals^12‐14. In mice, the H–2-associated resistance to leukaemia is at the second level and is probably an example of immune surveillance, in which the immune system eliminates or prevents the multiplication of nascent malignant cells^14–16. Possible effector mechanisms for immune surveillance which have been described include cytotoxic cells¹⁷, antibody¹⁸ or non-lymphoid cells^19,20. An alternative to immune surveillance is that genetic resistance may be expressed directly by the target cells, involving resistance either to viral infection²¹ or to malignant transformation. We have used transfers of bursal cells from genetically resistant chickens into bursa-lymphocyte-depleted genetically susceptible chickens, and vice versa, to show that genetic resistance to lymphoid leukosis resides in the bursal target cell, and that neither non-B cells nor cooperation between non-B cells and B cells has a role in this resistance.