PMID- 12727647
OWN - NLM
STAT- MEDLINE
DCOM- 20030619
LR  - 20220408
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 987
DP  - 2003 Apr
TI  - The role of relB in regulating the adaptive immune response.
PG  - 249-57
AB  - 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-kappaB 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.
FAU - Zanetti, Maurizio
AU  - Zanetti M
AD  - Department of Medicine and the Cancer Center, University of California, San 
      Diego, La Jolla, California 92093-0837, USA. mzanetti@ucsd.edu
FAU - Castiglioni, Paola
AU  - Castiglioni P
FAU - Schoenberger, Stephen
AU  - Schoenberger S
FAU - Gerloni, Mara
AU  - Gerloni M
LA  - eng
GR  - R01 CA77427/CA/NCI NIH HHS/United States
GR  - R21 AI49774/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Relb protein, mouse)
RN  - 0 (Transcription Factors)
RN  - 147337-75-5 (Transcription Factor RelB)
SB  - IM
MH  - Adaptation, Physiological/*physiology
MH  - Animals
MH  - Immunity, Cellular/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Proto-Oncogene Proteins/*physiology
MH  - T-Lymphocytes, Cytotoxic/immunology
MH  - Transcription Factor RelB
MH  - Transcription Factors/*physiology
RF  - 32
EDAT- 2003/05/03 05:00
MHDA- 2003/06/20 05:00
CRDT- 2003/05/03 05:00
PHST- 2003/05/03 05:00 [pubmed]
PHST- 2003/06/20 05:00 [medline]
PHST- 2003/05/03 05:00 [entrez]
AID - 10.1111/j.1749-6632.2003.tb06056.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2003 Apr;987:249-57. doi: 10.1111/j.1749-6632.2003.tb06056.x.