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Graft-versus-host disease is one of the major problems in clinical bone marrow transplantation. Many experiments in animals have shown that it could be greatly reduced if mature T lymphocytes were removed from the donor marrow. Here we describe a new rat monoclonal antibody, CAMPATH 1, which is suitable for depleting lymphocytes from human marrow grafts. CAMPATH 1 is an IgM that fixes human complement. It binds to both T and B lymphocytes and some monocytes but not to other hemopoietic cells. When peripheral blood mononuclear cells were treated with CAMPATH 1 and complement, more than 99% of lymphocytes were killed and viable T cells could no longer be detected. Under these conditions, in vitro multipotential erythroid and myeloid colony-forming cells were unaffected. As well as being used for in vitro treatment of bone marrow to remove T cells, CAMPATH 1 could potentially be applied to other experimental and clinical situations where depletion of lymphoid cells is required, including serotherapy to achieve immunosuppression for organ transplants or to treat lymphocytic leukemias.

Further mapping of the mouse T-cell factor specific for poly(Try,Glu)-polyD-LAla--polyLys is reported. It is shown to be a product of the I-A subregion of the H-2 complex by the use of antisera either raised specifically against or made specific, by absorption, for different regions of the H-2 complex. The factor cooperates across allogeneic barriers, e.g., when factor produced by one strian is combined with bone marrow cells of other H-2 incompatible strains.

L ], 1 a n d s u b s e q u e n t l y c u l t u r e d briefly in vitro, release a soluble factor c a p a b l e of r e p l a c i n g t h y m u s -d e r i v e d (T) cells in the t h y m u s -d e p e n d e n t a n t i b o d y response to ( T , G ) -A --L of b o n e m a r r o w -d e r i v e d (B) cells in i r r a d i a t e d r e c i p i e n t s (1). T h i s factor was n o t r e m o v e d by a n t i -i m m u n o g l o b u l i n sera ( a n t i m o u s e F a b ) , b u t wasc o m p l e t e l y a d s o r b e d by a l l o a n t i s e r a raised a g a i n s t the H -2 t y p e of the s t r a i n p r o d u c i n g the factor (2). We now report f u r t h e r c h a r a c t e r i z a t i o n a n d m a p p i n g of this T -c e l l factor.

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