The radiation-sensitive costimulatory factors involved in B-cell-dependent T-cell activation by minor lymphocyte stimulating antigen
| Autor: | Kenneth S.S. Chang, Shwu-Fen Jiang, Kai-Ping N. Chow, Charles C. Y. Shih, Hong-Sheng Kong, Jin-Bau Fu |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Immunoconjugates
T-Lymphocytes Endocrinology Diabetes and Metabolism Lymphocyte T cell Clinical Biochemistry Naive B cell Antigen-Presenting Cells Mice Inbred Strains chemical and pharmacologic phenomena Lymphocyte Activation Radiation Tolerance Minor Lymphocyte Stimulatory Antigens Abatacept Mice CD28 Antigens Antigen Antigens CD medicine Animals CTLA-4 Antigen Pharmacology (medical) Antigen-presenting cell Molecular Biology Cells Cultured B cell B-Lymphocytes CD40 biology Biochemistry (medical) CD28 hemic and immune systems Cell Biology General Medicine Intercellular Adhesion Molecule-1 Antigens Differentiation Molecular biology Lymphocyte Function-Associated Antigen-1 medicine.anatomical_structure B7-1 Antigen biology.protein Cytokines Lymphocyte Culture Test Mixed |
| Zdroj: | Journal of Biomedical Science. 5:332-342 |
| ISSN: | 1423-0127 1021-7770 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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