PMID- 16081792
OWN - NLM
STAT- MEDLINE
DCOM- 20051130
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 175
IP  - 4
DP  - 2005 Aug 15
TI  - Enhancement of dendritic cell antigen cross-presentation by CpG DNA involves type 
      I IFN and stabilization of class I MHC mRNA.
PG  - 2244-51
AB  - Dendritic cells (DCs) internalize exogenous Ags and process them for 
      cross-presentation by class I MHC (MHC-I) to CD8+ T cells. This processing can 
      occur by transporter for Ag presentation (TAP)-dependent or TAP-independent 
      mechanisms. We observed that CpG DNA enhanced cross-presentation of Ags by 
      Flt-3L-cultured bone marrow-derived murine DCs by a type I IFN 
      (IFN-alphabeta)-dependent mechanism. Myeloid DCs provided cross-presentation 
      function in this system. Both TAP1 knockout and wild-type DCs showed enhanced 
      cross-presentation when treated with CpG DNA at 26 degrees C, demonstrating that 
      TAP is not essential to this regulatory mechanism, although TAP is an important 
      determinant of MHC-I expression. Enhancement of cross-processing by CpG DNA did 
      not involve increased Ag uptake or proteolysis but did correlate with 
      IFN-alphabeta-dependent increases in expression of MHC-I mRNA and protein. 
      Increased MHC-I mRNA levels resulted in part from stabilization of MHC-I mRNA, a 
      novel posttranscriptional mechanism for regulation of MHC-I expression. Thus, a 
      major mechanism by which CpG oligodeoxynucleotide increase cross presentation by 
      DCs appears to be an IFN-alphabeta-mediated increase in MHC-I synthesis.
FAU - Kuchtey, John
AU  - Kuchtey J
AD  - Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, 
      USA.
FAU - Chefalo, Peter J
AU  - Chefalo PJ
FAU - Gray, Reginald C
AU  - Gray RC
FAU - Ramachandra, Lakshmi
AU  - Ramachandra L
FAU - Harding, Clifford V
AU  - Harding CV
LA  - eng
GR  - AI055793/AI/NIAID NIH HHS/United States
GR  - AI34343/AI/NIAID NIH HHS/United States
GR  - AI36219/AI/NIAID NIH HHS/United States
GR  - AI47255/AI/NIAID NIH HHS/United States
GR  - P30 CA43703/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 2)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (CPG-oligonucleotide)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Interferon-alpha)
RN  - 0 (Oligodeoxyribonucleotides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tap1 protein, mouse)
RN  - 77238-31-4 (Interferon-beta)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 2
MH  - ATP-Binding Cassette Transporters/biosynthesis/genetics
MH  - Adjuvants, Immunologic/*pharmacology
MH  - Animals
MH  - Cells, Cultured
MH  - CpG Islands/immunology
MH  - *Cross-Priming/genetics
MH  - Dendritic Cells/*immunology/metabolism
MH  - Half-Life
MH  - Histocompatibility Antigens Class I/*genetics/metabolism
MH  - Interferon-alpha/biosynthesis/*physiology
MH  - Interferon-beta/biosynthesis/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oligodeoxyribonucleotides/*pharmacology
MH  - Ovalbumin/immunology/metabolism
MH  - *RNA Stability/genetics/immunology
MH  - RNA, Messenger/*metabolism
MH  - Signal Transduction/genetics/immunology
MH  - Up-Regulation/genetics/immunology
EDAT- 2005/08/06 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/08/06 09:00
PHST- 2005/08/06 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/08/06 09:00 [entrez]
AID - 175/4/2244 [pii]
AID - 10.4049/jimmunol.175.4.2244 [doi]
PST - ppublish
SO  - J Immunol. 2005 Aug 15;175(4):2244-51. doi: 10.4049/jimmunol.175.4.2244.