AUGMENTATION OF INTESTINAL AND PERIPHERAL NATURAL KILLER CELL ACTIVITY DURING THE GRAFT-VERSUS-HOST REACTION IN MICE

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Abstract
The possibility that nonspecific cytotoxicity may be involved in the pathogenesis of the intestinal phase of the graft-vs.-host reaction (GVHR) was investigated in mice. A GVHR was induced in unirradiated (CBA .times. BALB/c)F1 mice and natural killer (NK) cell activity against YAC-1 [mouse lymphoma cells] followed in the spleen, mesenteric lymph node (MLN), and isolated intraepithelial lymphocytes (IEL). Augmented NK activity developed simultaneously in all tissues in parallel with the progress of the GVHR. The NK activity of IEL also showed a close association with the increased numbers of IEF found on sections of small intestine. Mature T lymphocytes and macrophages did not contribute to the nonspecific cytotoxicity, and antihost cytotoxic T cells were not detected in any tissue. Generalized recruitment of NK cells occurs during the GVHR both in peripheral and intestinal lymphoid tissues. Lymphokines are probably responsible for this phenomenon. NK cells recruited by a delayed-type hypersensitivity reaction may contribute to the pathogenesis of the GVHR, but an alternative explanation is that NK cells may inhibit the progression of the GVHR.

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