In vivo generation and function of CD21high IGMHIGH (MZ) B cells is BTK dependent and T independent

F. Martin, Alyce M. Oliver, J. F. Kearney

Research output: Contribution to journalArticle

Abstract

Newly formed B cells can go to the splenic follicular or marginal zone but the factors affecting this choice are not known. We have followed the in vivo generation and functional capabilities of a cohort of identical B cell (Id+) clones that is enriched in the CD21highIgHIGH marginal zone (MZ) B cell repertoire of the VH81X transgenic (tg) mouse. Although the number of Id+cells generated in the bone marrow of tg, tg CD40LT and tg xid mice is comparable, in only the first two these cells are enriched in the MZ. Tg xid mice are able to generate reduced numbers of MZ Id+ cells with phenotype and lifespan similar to normal MZ B cells, however these cells do not respond to an in vivo T independent (TI) antigenic stimulation by heat killed S. Pneumoniae vaccine. MZ B cells generated plasmablasts after challenge in both tg and tg CD40LT mice Id+ beginning at 24 hrs and peaking at 3-4 days while in the tg xid they did not. These data suggest that due to their btk-dependent signaling defect tg xid mice develop two malfunctions of the B cell compartment: first he inability to generate normal numbers of MZ Id+ effector cells and second the cells that are generated do not respond to the antigenic challenge.

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998
Externally publishedYes

Fingerprint

B-lymphocytes
B-Lymphocytes
Cells
genetically modified organisms
Transgenic Mice
mice
Clone cells
cells
Bone
Vaccines
Pneumonia
Clone Cells
Cell Count
Hot Temperature
Bone Marrow
Defects
bone marrow
pneumonia
Phenotype
clones

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

In vivo generation and function of CD21high IGMHIGH (MZ) B cells is BTK dependent and T independent. / Martin, F.; Oliver, Alyce M.; Kearney, J. F.

In: FASEB Journal, Vol. 12, No. 5, 20.03.1998.

Research output: Contribution to journalArticle

@article{fac32acc9efc46c388385f86d67c79a7,
title = "In vivo generation and function of CD21high IGMHIGH (MZ) B cells is BTK dependent and T independent",
abstract = "Newly formed B cells can go to the splenic follicular or marginal zone but the factors affecting this choice are not known. We have followed the in vivo generation and functional capabilities of a cohort of identical B cell (Id+) clones that is enriched in the CD21highIgHIGH marginal zone (MZ) B cell repertoire of the VH81X transgenic (tg) mouse. Although the number of Id+cells generated in the bone marrow of tg, tg CD40LT and tg xid mice is comparable, in only the first two these cells are enriched in the MZ. Tg xid mice are able to generate reduced numbers of MZ Id+ cells with phenotype and lifespan similar to normal MZ B cells, however these cells do not respond to an in vivo T independent (TI) antigenic stimulation by heat killed S. Pneumoniae vaccine. MZ B cells generated plasmablasts after challenge in both tg and tg CD40LT mice Id+ beginning at 24 hrs and peaking at 3-4 days while in the tg xid they did not. These data suggest that due to their btk-dependent signaling defect tg xid mice develop two malfunctions of the B cell compartment: first he inability to generate normal numbers of MZ Id+ effector cells and second the cells that are generated do not respond to the antigenic challenge.",
author = "F. Martin and Oliver, {Alyce M.} and Kearney, {J. F.}",
year = "1998",
month = "3",
day = "20",
language = "English (US)",
volume = "12",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "5",

}

TY - JOUR

T1 - In vivo generation and function of CD21high IGMHIGH (MZ) B cells is BTK dependent and T independent

AU - Martin, F.

AU - Oliver, Alyce M.

AU - Kearney, J. F.

PY - 1998/3/20

Y1 - 1998/3/20

N2 - Newly formed B cells can go to the splenic follicular or marginal zone but the factors affecting this choice are not known. We have followed the in vivo generation and functional capabilities of a cohort of identical B cell (Id+) clones that is enriched in the CD21highIgHIGH marginal zone (MZ) B cell repertoire of the VH81X transgenic (tg) mouse. Although the number of Id+cells generated in the bone marrow of tg, tg CD40LT and tg xid mice is comparable, in only the first two these cells are enriched in the MZ. Tg xid mice are able to generate reduced numbers of MZ Id+ cells with phenotype and lifespan similar to normal MZ B cells, however these cells do not respond to an in vivo T independent (TI) antigenic stimulation by heat killed S. Pneumoniae vaccine. MZ B cells generated plasmablasts after challenge in both tg and tg CD40LT mice Id+ beginning at 24 hrs and peaking at 3-4 days while in the tg xid they did not. These data suggest that due to their btk-dependent signaling defect tg xid mice develop two malfunctions of the B cell compartment: first he inability to generate normal numbers of MZ Id+ effector cells and second the cells that are generated do not respond to the antigenic challenge.

AB - Newly formed B cells can go to the splenic follicular or marginal zone but the factors affecting this choice are not known. We have followed the in vivo generation and functional capabilities of a cohort of identical B cell (Id+) clones that is enriched in the CD21highIgHIGH marginal zone (MZ) B cell repertoire of the VH81X transgenic (tg) mouse. Although the number of Id+cells generated in the bone marrow of tg, tg CD40LT and tg xid mice is comparable, in only the first two these cells are enriched in the MZ. Tg xid mice are able to generate reduced numbers of MZ Id+ cells with phenotype and lifespan similar to normal MZ B cells, however these cells do not respond to an in vivo T independent (TI) antigenic stimulation by heat killed S. Pneumoniae vaccine. MZ B cells generated plasmablasts after challenge in both tg and tg CD40LT mice Id+ beginning at 24 hrs and peaking at 3-4 days while in the tg xid they did not. These data suggest that due to their btk-dependent signaling defect tg xid mice develop two malfunctions of the B cell compartment: first he inability to generate normal numbers of MZ Id+ effector cells and second the cells that are generated do not respond to the antigenic challenge.

UR - http://www.scopus.com/inward/record.url?scp=33749344943&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749344943&partnerID=8YFLogxK

M3 - Article

VL - 12

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 5

ER -