The Radiation-Sensitive Costimulatory Factors Involved in B-Cell-Dependent T-Cell Activation by Minor Lymphocyte Stimulating Antigen

• Published in: Journal of biomedical science Vol. 5; no. 5; pp. 332 - 342
• Main Authors: Chow, Kai-Ping N., Fu, Jin-Bau, Kong, Hong-Sheng, Jiang, Shwu-Fen, Chang, Kenneth S.S., Shih, Charles C.-Y.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland 01.05.1998
• Subjects: Original Paper; Radiosensitivity; B7; Costimulation; T-cell activation
• ISSN: 1021-7770; 1423-0127
• DOI: 10.1159/000025347

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.