PMID- 14734734
OWN - NLM
STAT- MEDLINE
DCOM- 20040507
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 172
IP  - 3
DP  - 2004 Feb 1
TI  - Autoreactive B cells in lupus-prone New Zealand black mice exhibit aberrant 
      survival and proliferation in the presence of self-antigen in vivo.
PG  - 1553-60
AB  - To identify defects in B cell tolerance that may contribute to the production of 
      autoantibodies in New Zealand Black (NZB) mice, we crossed soluble hen egg white 
      lysozyme (sHEL) and anti-HEL Ig transgenes (Ig Tg) onto the NZB background. In 
      this study, we have examined one of the first checkpoints involved in maintenance 
      of peripheral B cell tolerance, follicular exclusion and elimination of 
      self-reactive B cells in the absence of T cell help. Freshly isolated anti-HEL Ig 
      Tg B cells were labeled with CFSE, adoptively transferred into sHEL recipients, 
      and the fate of self-reactive anti-HEL Ig Tg B cells was followed using flow 
      cytometry and immunofluorescence microscopy. Although anti-HEL Ig Tg B cells from 
      NZB mice are appropriately excluded from B cell follicles in NZB sHEL recipient 
      mice, they demonstrate aberrant survival, proliferation, and generation of 
      anti-HEL Ab-producing cells. This abnormal response results from an intrinsic 
      defect in NZB B cells, requires the presence of CD4(+) T cells, and is 
      facilitated by the splenic environment in NZB mice. Thus, NZB mice have immune 
      defects that interact synergistically to allow autoreactive B cells to become 
      activated despite the presence of tolerizing autoantigens.
FAU - Chang, Nan-Hua
AU  - Chang NH
AD  - Arthritis Centre of Excellence, Toronto Western Research Institute, Toronto, 
      Ontario, Canada.
FAU - MacLeod, Ralph
AU  - MacLeod R
FAU - Wither, Joan E
AU  - Wither JE
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Autoantibodies)
RN  - 0 (Immunoglobulin Heavy Chains)
RN  - EC 3.2.1.- (hen egg lysozyme)
RN  - EC 3.2.1.17 (Muramidase)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Autoantibodies/*biosynthesis
MH  - B-Lymphocyte Subsets/*immunology/*metabolism/pathology/transplantation
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - Cell Differentiation/genetics/immunology
MH  - Cell Division/genetics/immunology
MH  - Cell Survival/genetics/immunology
MH  - Chickens
MH  - Crosses, Genetic
MH  - Immunoglobulin Heavy Chains/genetics/immunology
MH  - Interphase/genetics/immunology
MH  - Lupus Erythematosus, Systemic/genetics/*immunology/pathology
MH  - Lymphocyte Activation/genetics
MH  - Major Histocompatibility Complex/genetics/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred NZB
MH  - Mice, Transgenic
MH  - Muramidase/genetics/immunology
MH  - Self Tolerance/genetics/*immunology
MH  - Transgenes/immunology
EDAT- 2004/01/22 05:00
MHDA- 2004/05/08 05:00
CRDT- 2004/01/22 05:00
PHST- 2004/01/22 05:00 [pubmed]
PHST- 2004/05/08 05:00 [medline]
PHST- 2004/01/22 05:00 [entrez]
AID - 10.4049/jimmunol.172.3.1553 [doi]
PST - ppublish
SO  - J Immunol. 2004 Feb 1;172(3):1553-60. doi: 10.4049/jimmunol.172.3.1553.