The Role of relB in Regulating the Adaptive Immune Response

: Dendritic cells (DCs), which represent a key type of antigen‐presenting cell (APC), are important for the development of innate and adaptive immunity. DCs are involved in T cell activation in at least two main ways: priming via direct processing/presentation of soluble antigen taken up from the mi...

Full description

Saved in:
Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2003-04, Vol.987 (1), p.249-257
Main Authors: ZANETTI, MAURIZIO, CASTIGLIONI, PAOLA, SCHOENBERGER, STEPHEN, GERLONI, MARA
Format: Article
Language:English
Subjects:
Adaptation, Physiological - physiology
Animals
cross-priming
dendritic cells
Immunity, Cellular - physiology
Mice
Mice, Inbred C57BL
Proto-Oncogene Proteins - physiology
relB
T cell priming
T-Lymphocytes, Cytotoxic - immunology
Transcription Factor RelB
Transcription Factors - physiology
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:: Dendritic cells (DCs), which represent a key type of antigen‐presenting cell (APC), are important for the development of innate and adaptive immunity. DCs are involved in T cell activation in at least two main ways: priming via direct processing/presentation of soluble antigen taken up from the microenvironment (conventional priming), and processing/presentation of antigen released from other cells (cross‐priming). relB, a component of the NF‐κB complex of transcription factors, is a critical regulator of the differentiation of DCs. In mice, lack of relB impairs DCs derived from bone marrow both in number and function. Here relB (−/−) bone marrow chimera mice is used to study the APC function of residual DCs in presentation of soluble antigen and cross‐priming. It is found that the DCs in these mice are profoundly deficient in their ability to both prime and cross‐prime T cell responses. It was concluded that the relB gene is involved in regulating the APC function of DCs in vivo.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2003.tb06056.x