Work in this laboratory has been directed toward the understanding of the pathogenesis of allogenic HVG syndrome, a disease of altered immunity which may follow the perinatal inoculation of semiallogenic lymphohemopoietic cells into susceptible strains of inbred mice. Work completed has shown that the main pathologic features of the disease are T cell depletion, B cell hyperplasia and immune complex formation. The specific aims of the proposal include: 1. To ascertain the role and fate of labelled F1 hybrid T cells after their inoculation into RFM hosts. 2. To identify the cells present in the spleens of RFM perinates which can recognize and react against donor F1 cells, with emphasis on T and NK cells. 3. To study the mechanism(s) by which F1 donor and host T cells are lost during the HVG reaction, and whether there is a differential sensitivity of T cell subsets to loss during the allogenic reaction which can be correlated with the marked serum changes observed. Histopathologic, cytologic, cytogenetic and in vitro culture techniques will be used. Successful completion of the work should yield important information directly applicable to the mechanisms of clinical bone marrow graft rejection, acute and chronic Graft Versus Host syndromes, tolerance and the cellular changes which favor the formation of nephropathic immune complexes.