title: Nuclear localization of RelB is associated with effective antigen-presenting cell function.
abstract: Dendritic cells (DC) are potent APCs that enter resting tissues as precursors and, after Ag exposure, differentiate and migrate to draining lymph nodes. The phenotype of RelB knockout mice implicates this member of the NF kappa B/Rel family in DC differentiation. To further elucidate the role of RelB in DC differentiation, mRNA, intracellular protein expression, and DNA binding activity of RelB were examined in immature and differentiated human DC, as well as other PB mononuclear cell populations. RelB protein and mRNA were detected constitutively in lymphocytes and in activated monocytes, differentiated DC, and monocyte-derived DC. Immunohistochemical staining demonstrated RelB within the differentiated lymph node interdigitating DC and follicular DC, but not undifferentiated DC in normal skin. Active nuclear RelB was detected by supershift assay only in differentiated DC derived from either PB precursors or monocytes and in activated B cells. These RelB+ APC were potent stimulators of the MLR. The data indicate that RelB expression is regulated both transcriptionally and post-translationally in myeloid cells. Within the nucleus, RelB may specifically transactivate genes that are critical for APC function.
authors.affiliation: Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Australia.
authors.forename: A R
authors.initials: AR
authors.lastname: Pettit
authors.forename: C
authors.initials: C
authors.lastname: Quinn
authors.forename: K P
authors.initials: KP
authors.lastname: MacDonald
authors.forename: L L
authors.initials: LL
authors.lastname: Cavanagh
authors.forename: G
authors.initials: G
authors.lastname: Thomas
authors.forename: W
authors.initials: W
authors.lastname: Townsend
authors.forename: M
authors.initials: M
authors.lastname: Handel
authors.forename: R
authors.initials: R
authors.lastname: Thomas
mesh_terms: D000328:Adult; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000276:immunology; D002454:Cell Differentiation; D002467:Cell Nucleus / Q000276:immunology* / Q000378:metabolism*; D003713:Dendritic Cells / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007399:Interphase; D008198:Lymph Nodes / Q000166:cytology / Q000378:metabolism; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000166:cytology / Q000378:metabolism; D051379:Mice; D009000:Monocytes / Q000378:metabolism; D011518:Proto-Oncogene Proteins; D011817:Rabbits; D063268:Sialic Acid Binding Ig-like Lectin 3; D051841:Transcription Factor RelB; D014157:Transcription Factors / Q000096:biosynthesis / Q000276:immunology* / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; C571163:CD33 protein, human; C571165:Cd33 protein, mouse; D011518:Proto-Oncogene Proteins; C497593:RELB protein, human; C497594:Relb protein, mouse; D063268:Sialic Acid Binding Ig-like Lectin 3; D014157:Transcription Factors; D051841:Transcription Factor RelB