The effect of chronic graft-versus-host disease on b cell development

Kathy L. Schreiber, James Forman

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Chronic graft-versus-host disease often results in a combined deficiency of humoral and cell-mediated immunity. Clinical and experimental studies have suggested that the decrease in B cell responsiveness is due to a failure of B cell production in the bone marrow, intrinsic B cell defects, excessive suppressor T cell activity, and deficient T helper activity. In the present study, we analyze the basis of B cell immunodeficiency in C.B-20→(C.B-20×B10.D2)Fi animals afflicted with chronic GVHD. The initial decline in B cell production in the BM accounts for the early reduction in the number of B cells in the spleen and BM. Later, as B cells appear in near-normal numbers in the BM, the spleen and lymph node are repopulated by the newly derived B cells. Associated with the appearance of B cells in the BM and spleen is the ability to respond to lipopolysaccharide. In contrast, both B cell populations are severely diminished in their ability to proliferate in response to agar-derived mitogens to form colonies (CFU-B). The reduction in the CFU-B response is most likely a consequence of an inherent B cell defect, since purification of C.B-20→Fi splenic B cells does not restore the colonyforming potential. Unlike BM and splenic B cells, LN B cells are unable to respond to either mitogen. Taken together, these results imply that a population of B cells derived from a distinct lineage and/or B cell maturation is defective in mice undergoing GVHD.

Original languageEnglish (US)
Pages (from-to)597-604
Number of pages8
JournalTransplantation
Volume55
Issue number3
StatePublished - Jan 1 1993

Fingerprint

Graft vs Host Disease
B-Lymphocytes
Spleen
Mitogens
Cellular Immunity
Population
Agar
Lipopolysaccharides

ASJC Scopus subject areas

  • Transplantation

Cite this

The effect of chronic graft-versus-host disease on b cell development. / Schreiber, Kathy L.; Forman, James.

In: Transplantation, Vol. 55, No. 3, 01.01.1993, p. 597-604.

Research output: Contribution to journalArticle

@article{007abc784813452e8e5f98021ee36e8c,
title = "The effect of chronic graft-versus-host disease on b cell development",
abstract = "Chronic graft-versus-host disease often results in a combined deficiency of humoral and cell-mediated immunity. Clinical and experimental studies have suggested that the decrease in B cell responsiveness is due to a failure of B cell production in the bone marrow, intrinsic B cell defects, excessive suppressor T cell activity, and deficient T helper activity. In the present study, we analyze the basis of B cell immunodeficiency in C.B-20→(C.B-20×B10.D2)Fi animals afflicted with chronic GVHD. The initial decline in B cell production in the BM accounts for the early reduction in the number of B cells in the spleen and BM. Later, as B cells appear in near-normal numbers in the BM, the spleen and lymph node are repopulated by the newly derived B cells. Associated with the appearance of B cells in the BM and spleen is the ability to respond to lipopolysaccharide. In contrast, both B cell populations are severely diminished in their ability to proliferate in response to agar-derived mitogens to form colonies (CFU-B). The reduction in the CFU-B response is most likely a consequence of an inherent B cell defect, since purification of C.B-20→Fi splenic B cells does not restore the colonyforming potential. Unlike BM and splenic B cells, LN B cells are unable to respond to either mitogen. Taken together, these results imply that a population of B cells derived from a distinct lineage and/or B cell maturation is defective in mice undergoing GVHD.",
author = "Schreiber, {Kathy L.} and James Forman",
year = "1993",
month = "1",
day = "1",
language = "English (US)",
volume = "55",
pages = "597--604",
journal = "Transplantation",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - The effect of chronic graft-versus-host disease on b cell development

AU - Schreiber, Kathy L.

AU - Forman, James

PY - 1993/1/1

Y1 - 1993/1/1

N2 - Chronic graft-versus-host disease often results in a combined deficiency of humoral and cell-mediated immunity. Clinical and experimental studies have suggested that the decrease in B cell responsiveness is due to a failure of B cell production in the bone marrow, intrinsic B cell defects, excessive suppressor T cell activity, and deficient T helper activity. In the present study, we analyze the basis of B cell immunodeficiency in C.B-20→(C.B-20×B10.D2)Fi animals afflicted with chronic GVHD. The initial decline in B cell production in the BM accounts for the early reduction in the number of B cells in the spleen and BM. Later, as B cells appear in near-normal numbers in the BM, the spleen and lymph node are repopulated by the newly derived B cells. Associated with the appearance of B cells in the BM and spleen is the ability to respond to lipopolysaccharide. In contrast, both B cell populations are severely diminished in their ability to proliferate in response to agar-derived mitogens to form colonies (CFU-B). The reduction in the CFU-B response is most likely a consequence of an inherent B cell defect, since purification of C.B-20→Fi splenic B cells does not restore the colonyforming potential. Unlike BM and splenic B cells, LN B cells are unable to respond to either mitogen. Taken together, these results imply that a population of B cells derived from a distinct lineage and/or B cell maturation is defective in mice undergoing GVHD.

AB - Chronic graft-versus-host disease often results in a combined deficiency of humoral and cell-mediated immunity. Clinical and experimental studies have suggested that the decrease in B cell responsiveness is due to a failure of B cell production in the bone marrow, intrinsic B cell defects, excessive suppressor T cell activity, and deficient T helper activity. In the present study, we analyze the basis of B cell immunodeficiency in C.B-20→(C.B-20×B10.D2)Fi animals afflicted with chronic GVHD. The initial decline in B cell production in the BM accounts for the early reduction in the number of B cells in the spleen and BM. Later, as B cells appear in near-normal numbers in the BM, the spleen and lymph node are repopulated by the newly derived B cells. Associated with the appearance of B cells in the BM and spleen is the ability to respond to lipopolysaccharide. In contrast, both B cell populations are severely diminished in their ability to proliferate in response to agar-derived mitogens to form colonies (CFU-B). The reduction in the CFU-B response is most likely a consequence of an inherent B cell defect, since purification of C.B-20→Fi splenic B cells does not restore the colonyforming potential. Unlike BM and splenic B cells, LN B cells are unable to respond to either mitogen. Taken together, these results imply that a population of B cells derived from a distinct lineage and/or B cell maturation is defective in mice undergoing GVHD.

UR - http://www.scopus.com/inward/record.url?scp=0027532337&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027532337&partnerID=8YFLogxK

M3 - Article

C2 - 8456480

AN - SCOPUS:0027532337

VL - 55

SP - 597

EP - 604

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 3

ER -