CCR1-deficient T cells demonstrate impaired allo-specific responses but maintain cytolytic function. To assess donor T-cell function in vivo, B2D2F1 mice received transplants from syngeneic (□) and allogeneic CCR1^+/+ (■), or CCR1^−/− (▩) donors as described in Figure 2. (A,B) Absence of CCR1 on donor cells reduces splenic T-cell expansion (A) and serum INFγ levels (B) at day 7 following SCT. (C,D) Allospecific proliferation (C) and INFγ production (D) were also reduced in vitro during a MLR with wild-type (■) or CCR1^−/− (▩) T cells and allogeneic B6D2F1 stimulators or with control media (■ or , respectively), as described in “Materials and methods.” (E) Cytotoxic function of splenic T cells after in vitro priming was determined by a chromium release assay using P-815 (H2^d) and EL-4 (H2^b) target cells as previously described (■, wild-type → P-815; ●, CCR1^−/− → P-815; ▴, wild-type → EL-4; and ◆, CCR1^−/− → EL-4). (F,G) No differences in proliferation between CCR1^+/+ (■) and CCR1^−/− (▩) T cells are evident following stimulation with ConA (F), whereas proliferation of CCR1^−/− T cells was significantly reduced following anti-CD3–CD28 stimulation; *P < .05 (G). Data are from 1 of at least 3 similar experiments and are presented as means plus or minus SEM.