Abstract
The regulation of CD28/B7 is important in T-cell activation. It has been argued that its aberrant expression is involved in the radiosensitivity of B- cell-stimulated T-cell response. Here, this possibility is studied in the mixed lymphocyte reaction (MLR) induced by minor lymphocyte-stimulating (Mls) antigen-presenting irradiated B cells. By using anti-CD28 antibody, the CD28/B7-2-, LFA-1/ICAM-1-dependent Mls-MLR was found to be restored. By flow cytometry, approximately 70% B cells were lost but with unaffected B7-2 expression, indicating that the moderate CD28 costimulation was caused by mortality of antigen presenting cells. Despite of costimulatory deficiency, T cells were shown primed. However, the expression of early activation markers CD25 and CD69, which was shown unaffected by B7/CD28 blocking, was found partially inhibited. To further understand the regulation, we examined the ICAM-1 expression, and found that it was again not altered on irradiated B cells. Thus, the radiation-induced rapid loss of resting B cells may be the basic mechanism causing insufficient costimulatory activity in radiosensitive B-T interaction. Furthermore, the presence of an element, other than B7-2 involving in controlling early T-cell response is suggested.
Original language | English |
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Pages (from-to) | 332-342 |
Number of pages | 11 |
Journal | Journal of Biomedical Science |
Volume | 5 |
Issue number | 5 |
DOIs | |
State | Published - 1998 |
Keywords
- B7
- Costimulation
- Radiosensitivity
- T-cell activation