Expression and distribution of CD11a/CD18 and CD54 during human T cell–B cell interactions

Interactions between intercellular adhesion molecule 1 (ICAM‐1, CD54) and leukocyte function–associated antigen 1 (LFA‐1, CD11a/CD18) play a critical role in T cell–B cell collaboration. The current experiments were carried out to determine the expression and distribution of these adhesion molecules on human peripheral T cells and B cells during T cell–B cell collaboration. Resting CD4 + T cells were largely ICAM‐1 negative, whereas immobilized anti‐CD3 monoclonal antibody (mAb) rapidly induced ICAM‐1 expression. By contrast, most B cells expressed ICAM‐1 before activation, and further increases in density were noted with stimulation. Both B cells and CD4 + T cells expressed LFA‐1 before activation, although the density on CD4 + T cells was considerably greater. A double staining method for electron microscopic analysis was developed that permitted analysis of the expression and distribution of ICAM‐1 to be assessed during T cell–B cell collaboration. Under the experimental conditions examined, B cells showed a uniform distribution of ICAM‐1. In contrast, ICAM‐1 was highly mobile on the surface of CD4 + T cells. If the T cells were not fixed, staining, even at 4°C, caused rapid redistribution of ICAM‐1 into aggregates. However, by fixing cells before the staining procedures, the distribution of ICAM‐1 on CD4 + T cells could be accurately assessed. Most (85%) of the fixed activated CD4 + T cells showed a uniform distribution of ICAM‐1. However, when activated CD4 + T cells were cocultured with B cells, redistribution of ICAM‐1 on CD4 + T cells but not B cells occurred, such that the majority (85%) was found at or immediately adjacent to the point of attachment to the B cells. No redistribution of LFA‐1 on either T cells or B cells was found. These findings suggest that rapid changes in density of ICAM‐1 expression and the mobility of ICAM‐1 on activated T cells may play a role in providing activation signals to B cells during T cell–B cell collaboration.