The efficacy of hematopoietic stem cell (HSC) therapy for cerebral infarction has been previously demonstrated. However, the lack of response in some patients has hindered its widespread use. To establish HSC therapy as a standard treatment, it is important to examine the causes of non-responsiveness. In this study, we aimed to identify the specifications of transplanted cells based on their therapeutic mechanisms to predict treatment success. We found that HSC therapy activates injured cerebral endothelial cells via gap junctions because cell adhesion between HSCs and the endothelium plays an essential role in cellular communication via gap junctions. The expression of the adhesion molecule integrin β2 (CD18) in CD34-positive (CD34⁺) cells was identified as critical for the therapeutic effect on cerebral infarction in a murine model. Cells with low CD18 expression exhibited a weaker therapeutic effect than cells with high CD18 expression, even when the same number of HSCs was administered. The expression of CD18 in CD34⁺ cells can be used as a specification marker for transplanted HSCs and is useful for identifying non-responders. Furthermore, quantification of CD18 expression is crucial for evaluating the cellular potential of cell-based therapies for diseases where therapeutic effects are mediated through cell adhesion.