PMID- 15922563
OWN - NLM
STAT- MEDLINE
DCOM- 20051019
LR  - 20071114
IS  - 0896-8411 (Print)
IS  - 0896-8411 (Linking)
VI  - 25
IP  - 1
DP  - 2005 Aug
TI  - Defects in differentiation of bone-marrow derived dendritic cells of the BB rat 
      are partly associated with IDDM2 (the lyp gene) and partly associated with other 
      genes in the BB rat background.
PG  - 46-56
AB  - BB rats develop various organ-specific autoimmune diseases, e.g. autoimmune 
      diabetes and thyroiditis and have proven important to dissect genetic factors 
      that govern autoimmune disease development. The lymphopenia (lyp) gene (iddm2) is 
      linked to autoimmune disease development and is a major genetic difference 
      between diabetes-resistant (DR) and diabetes-prone (DP) BB rats. To study the 
      effects of the lyp gene and other genes on dendritic cell (DC) differentiation 
      from bone-marrow precursors, such differentiation was studied in BB-DP, BB-DR, 
      Wistar and F344 control rats. DC of BB-DP rats showed a lower MHC class II 
      expression as compared to BB-DR, Wistar and F344 rats. LPS-maturation did not 
      restore this low MHC class II expression. DC of BB-DP rats also showed a poor 
      capability to terminally differentiate into mature T cell stimulatory DC under 
      the influence of LPS and produced significantly lower quantities of IL-10, yet 
      these aberrancies were also found in BB-DR rats but did not occur in control 
      rats. This study thus shows that various aberrancies exist in the differentiation 
      of myeloid DC from bone-marrow precursors in the BB rat model of organ-specific 
      autoimmunity. These aberrancies are multigenically determined and partly 
      associated with iddm2 (lyp gene) and partly associated with other genes in the BB 
      rat.
FAU - Sommandas, Vinod
AU  - Sommandas V
AD  - Department of Immunology, Erasmus MC, PO Box 1738, 3000 DR Rotterdam, The 
      Netherlands. vsommandas@erasmusmc.nl
FAU - Rutledge, Elizabeth A
AU  - Rutledge EA
FAU - Van Yserloo, Brian
AU  - Van Yserloo B
FAU - Fuller, Jessica
AU  - Fuller J
FAU - Lernmark, Ake
AU  - Lernmark A
FAU - Drexhage, Hemmo A
AU  - Drexhage HA
LA  - eng
GR  - AI42380/AI/NIAID NIH HHS/United States
GR  - DK 17047/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Autoimmun
JT  - Journal of autoimmunity
JID - 8812164
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Lipopolysaccharides)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
RN  - 207137-56-2 (Interleukin-4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - EC 3.6.1.- (Gimap5 protein, rat)
SB  - IM
MH  - Animals
MH  - *Bone Marrow Cells/immunology/pathology
MH  - Cell Differentiation/*genetics
MH  - Dendritic Cells/immunology/metabolism/*pathology
MH  - Diabetes Mellitus, Type 1/*genetics/immunology
MH  - GTP-Binding Proteins/biosynthesis/*genetics
MH  - *Genetic Predisposition to Disease
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
MH  - Histocompatibility Antigens Class II/biosynthesis/genetics
MH  - Interleukin-10/biosynthesis
MH  - Interleukin-12/biosynthesis
MH  - Interleukin-4/pharmacology
MH  - Lipopolysaccharides/immunology
MH  - Rats
MH  - Rats, Inbred BB
MH  - Rats, Inbred F344
MH  - T-Lymphocytes/physiology
EDAT- 2005/06/01 09:00
MHDA- 2005/10/20 09:00
CRDT- 2005/06/01 09:00
PHST- 2004/11/10 00:00 [received]
PHST- 2005/03/22 00:00 [revised]
PHST- 2005/03/31 00:00 [accepted]
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/10/20 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
AID - S0896-8411(05)00058-2 [pii]
AID - 10.1016/j.jaut.2005.03.008 [doi]
PST - ppublish
SO  - J Autoimmun. 2005 Aug;25(1):46-56. doi: 10.1016/j.jaut.2005.03.008.