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

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...

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Published inJournal 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
LanguageEnglish
Published Basel, Switzerland 01.05.1998
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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.
AbstractList 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.
Author Jiang, Shwu-Fen
Chang, Kenneth S.S.
Chow, Kai-Ping N.
Shih, Charles C.-Y.
Kong, Hong-Sheng
Fu, Jin-Bau
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Issue 5
Keywords Radiosensitivity
B7
Costimulation
T-cell activation
Language English
License Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
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