Trafficking and survival of CIK cells upon adoptive transfer. Lethally irradiated host allogeneic (Balb/c, H-2^d, n = 5) and syngeneic (FVB/N, H-2^q, n = 5) recipients were injected with 5 × 10⁶ FVB wild-type BM cells with 10 × 10⁶ CIK cells generated from luc⁺ FVB mice (L2G85). To compare GVHD development, 10 × 10⁶ L2G85 splenocytes were transplanted with BM cells (n = 5). (A) BLI of mice after transplantation. Donor-derived CIK cells in the allogeneic mice homed to and proliferated in secondary lymphoid organs, followed by the infiltration of gut and skin (top row), which was similar to GVHD progression (bottom row). However, in CIK cell–receiving mice, the speed of spread to peripheral tissue was slower and maximum peak signal from gut was lower than that in animals receiving fresh splenocytes. In syngeneic mice (middle row), there was no significant CIK cell proliferation and only a transient signal was observed on day 14 in cervical lymph nodes and abdomen. (B) Quantitation of photon emission of BLI. (C) Ex vivo imaging demonstrated compared with naive splenocytes, CIK cell homing to and proliferating in gastrointestinal tissues over time. (D) Histopathology of selected tissues on day 7 after transplantation. Magnification was ×200 or ×400 as indicated. Goblet cells (dashed arrow); crypt abscesses (solid arrow); lymphocytic infiltration surrounding the bile ducts (red arrow). (E) Mice receiving splenocytes (n = 3) or CIK cells (n = 3) were humanely killed on day 7 after BMT. GVHD histopathologic score was calculated on liver, small intestine, and large intestine damage on day 7 after BMT (CIK vs splenocytes, P = .002). Error bars represent SD.