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ABROGATION OF THE ALLOREACTIVE RESPONSES OF CADAVER DONOR INTESTINAL LYMPHOCYTES BY SURGICAL CAMPATH-1H EXPOSURE.
James M. Mathew, PhD , Werviston DeFaria MD , Tomoaki Kato MD , Manuel Carreno MD , Teresa Vallone MT , Bonnie Blomberg PhD , Laphalle Fuller PhD , Violet Esquenazi PhD , Joshua Miller MD and Andreas G. Tzakis, MD . University of Miami Surgery and Miami FL, USA, University of Miami & VA Medical Center, 33136, Microbiology & Immunology .

Recent reports have suggested that the donor gastrointestinal lymphocytes are potent mediators of graft versus host (GvH) reactivity that may contribute to post-transplant morbidity in intestinal transplantation. Therefore, we have tested the proliferative capabilities (MLR) of lymphocytes derived from cadaver donor small intestine and the draining lymph nodes, obtained before and about 6 hours after revascularization (pre- and post- R) with the recipients who had been either treated with Campath-1H or not so treated immediately pre-operatively.
It was observed that the cells isolated from intestinal mucosa, lamina propria and lymph nodes harvested pre-R reacted to both the recipient and third party lymphocytes with stimulation indices (SI) ranging from 8.6 to 194 (n=10). Similar post-R preparations in Campath-1H treated recipients reacted at significantly lower magnitude giving SI of 2.0 – 56.6 (p<0.01). Such reduction was not observed with post-R samples from patients not treated with Campath-1H. Lymphocytes from both proximal (jejunal) and distal (colic) regions gave similar alloreactive responses. Both the pre- and post- revascularization samples had similar cellular yields and flow cytometric profiles, suggesting that despite an early functional change there was no cellular or receptor loss by the short-term (6 hour) exposure to Campath-1H in the intestinal graft or associated lymph nodes once revascularization occurred. These results suggested that Campath-1H treatment of the recipient might bring about a drastic reduction in potential GvH reactivity by the donor intestinal immune cells.