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CD30-Mediated Regulation of Cell Adhesion Molecule Expression on Murine T Cells
Immune Network ; : 8-15, 2003.
Article en En | WPRIM | ID: wpr-146215
Biblioteca responsable: WPRO
ABSTRACT
BACKGROUND: CD30 is a member of TNF receptor family and expressed on lymphocytes and other hematopoietic cells following activation as well as Hodgkin and Reed- Sternberg cells in Hodgkin's lymphoma. In this study, CD30-mediated regulation of cell adhesion molecule expression on normal activated mouse T cells was investigated. METHODS: Mouse T cells were activated with anti-CD3 antibody for induction of CD30, which was cross-linked by immobilized anti-CD30 antibody. RESULTS: High level of CD30 expression on T cells was observed on day 5, but only little on day 3 even under culture condition resulting in an identical T cell proliferation, indicating that CD30 expression requires a prolonged stimulation up to 5 days. Cross-linking of CD30 alone altered neither proliferation nor apoptosis of normal activated T cells. Instead, CD30 appeared to promote cell adherence to culture substrate, and considerably upregulated ICAM-1 and, to a lesser extent, ICAM-2 expression on activated T cells, whereas CD2 and CD18 (LFA-1) expression was not affected. None of cytokines known as main regulators of ICAM-1 expression on tissue cells (IL 4, IFNgamma and TNFalpha) enhanced ICAM-1 expression in the absence of CD30 signals. On the other hand, addition of NF-kappaB inhibitor, PDTC (0.1 mM) completely abrogated the CD30-mediated upregulation of ICAM-1 expression, but not CD2 and ICAM-2 expression. CONCLUSION: This results support that CD30 upregulates ICAM-1 expression of T cell and such regulation is not mediated by higher cytokine production but NF-kappaB activation. Therefore, CD30 may play important roles in T-T or T-B cell interaction through regulation of ICAM-1, and -2 expression.
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Texto completo: 1 Índice: WPRIM Asunto principal: Enfermedad de Hodgkin / Linfocitos / Linfocitos T / Moléculas de Adhesión Celular / Adhesión Celular / Comunicación Celular / Regulación hacia Arriba / Citocinas / FN-kappa B / Apoptosis Límite: Animals / Humans Idioma: En Revista: Immune Network Año: 2003 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Asunto principal: Enfermedad de Hodgkin / Linfocitos / Linfocitos T / Moléculas de Adhesión Celular / Adhesión Celular / Comunicación Celular / Regulación hacia Arriba / Citocinas / FN-kappa B / Apoptosis Límite: Animals / Humans Idioma: En Revista: Immune Network Año: 2003 Tipo del documento: Article