B lymphocytes differentially influence acute and chronic allograft rejection in mice

David J. DiLillo, Robert Griffiths, Surya V. Seshan, Cynthia M. Magro, Phillip Ruiz, Thomas M. Coffman, Thomas F. Tedder

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

The relative contributions of B lymphocytes and plasma cells during allograft rejection remain unclear. Therefore, the effects of B cell depletion on acute cardiac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mAbs. Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmablasts and some plasma cells. B cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment prevented allograftspecific IgG production. Strikingly, CD19 mAb treatment significantly reduced renal allograft rejection and abrogated allograftspecific IgG development, whereas CD20 mAb treatment did not. By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation of adoptively transferred alloantigen-specific CD4+ T cells, demonstrating that B cells can also negatively regulate allograft rejection. Thereby, B cells can either positively or negatively regulate allograft rejection depending on the nature of the allograft and the intensity of the rejection response. Moreover, CD19 mAb may represent a new approach for depleting both B cells and plasma cells to concomitantly impair T cell activation, inhibit the generation of new allograft-specific Abs, or reduce preexisting allograft-specific Ab levels in transplant patients.

Original languageEnglish
Pages (from-to)2643-2654
Number of pages12
JournalJournal of Immunology
Volume186
Issue number4
DOIs
StatePublished - Feb 15 2011

Fingerprint

Allografts
B-Lymphocytes
Plasma Cells
Immunoglobulin G
T-Lymphocytes
Kidney
Skin
Isoantigens
Graft Rejection
Therapeutics
Transplants

ASJC Scopus subject areas

  • Immunology

Cite this

DiLillo, D. J., Griffiths, R., Seshan, S. V., Magro, C. M., Ruiz, P., Coffman, T. M., & Tedder, T. F. (2011). B lymphocytes differentially influence acute and chronic allograft rejection in mice. Journal of Immunology, 186(4), 2643-2654. https://doi.org/10.4049/jimmunol.1002983

B lymphocytes differentially influence acute and chronic allograft rejection in mice. / DiLillo, David J.; Griffiths, Robert; Seshan, Surya V.; Magro, Cynthia M.; Ruiz, Phillip; Coffman, Thomas M.; Tedder, Thomas F.

In: Journal of Immunology, Vol. 186, No. 4, 15.02.2011, p. 2643-2654.

Research output: Contribution to journalArticle

DiLillo, DJ, Griffiths, R, Seshan, SV, Magro, CM, Ruiz, P, Coffman, TM & Tedder, TF 2011, 'B lymphocytes differentially influence acute and chronic allograft rejection in mice', Journal of Immunology, vol. 186, no. 4, pp. 2643-2654. https://doi.org/10.4049/jimmunol.1002983
DiLillo, David J. ; Griffiths, Robert ; Seshan, Surya V. ; Magro, Cynthia M. ; Ruiz, Phillip ; Coffman, Thomas M. ; Tedder, Thomas F. / B lymphocytes differentially influence acute and chronic allograft rejection in mice. In: Journal of Immunology. 2011 ; Vol. 186, No. 4. pp. 2643-2654.
@article{effce92115c94224a3723595d22bc95e,
title = "B lymphocytes differentially influence acute and chronic allograft rejection in mice",
abstract = "The relative contributions of B lymphocytes and plasma cells during allograft rejection remain unclear. Therefore, the effects of B cell depletion on acute cardiac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mAbs. Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmablasts and some plasma cells. B cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment prevented allograftspecific IgG production. Strikingly, CD19 mAb treatment significantly reduced renal allograft rejection and abrogated allograftspecific IgG development, whereas CD20 mAb treatment did not. By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation of adoptively transferred alloantigen-specific CD4+ T cells, demonstrating that B cells can also negatively regulate allograft rejection. Thereby, B cells can either positively or negatively regulate allograft rejection depending on the nature of the allograft and the intensity of the rejection response. Moreover, CD19 mAb may represent a new approach for depleting both B cells and plasma cells to concomitantly impair T cell activation, inhibit the generation of new allograft-specific Abs, or reduce preexisting allograft-specific Ab levels in transplant patients.",
author = "DiLillo, {David J.} and Robert Griffiths and Seshan, {Surya V.} and Magro, {Cynthia M.} and Phillip Ruiz and Coffman, {Thomas M.} and Tedder, {Thomas F.}",
year = "2011",
month = "2",
day = "15",
doi = "10.4049/jimmunol.1002983",
language = "English",
volume = "186",
pages = "2643--2654",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "4",

}

TY - JOUR

T1 - B lymphocytes differentially influence acute and chronic allograft rejection in mice

AU - DiLillo, David J.

AU - Griffiths, Robert

AU - Seshan, Surya V.

AU - Magro, Cynthia M.

AU - Ruiz, Phillip

AU - Coffman, Thomas M.

AU - Tedder, Thomas F.

PY - 2011/2/15

Y1 - 2011/2/15

N2 - The relative contributions of B lymphocytes and plasma cells during allograft rejection remain unclear. Therefore, the effects of B cell depletion on acute cardiac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mAbs. Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmablasts and some plasma cells. B cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment prevented allograftspecific IgG production. Strikingly, CD19 mAb treatment significantly reduced renal allograft rejection and abrogated allograftspecific IgG development, whereas CD20 mAb treatment did not. By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation of adoptively transferred alloantigen-specific CD4+ T cells, demonstrating that B cells can also negatively regulate allograft rejection. Thereby, B cells can either positively or negatively regulate allograft rejection depending on the nature of the allograft and the intensity of the rejection response. Moreover, CD19 mAb may represent a new approach for depleting both B cells and plasma cells to concomitantly impair T cell activation, inhibit the generation of new allograft-specific Abs, or reduce preexisting allograft-specific Ab levels in transplant patients.

AB - The relative contributions of B lymphocytes and plasma cells during allograft rejection remain unclear. Therefore, the effects of B cell depletion on acute cardiac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mAbs. Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmablasts and some plasma cells. B cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment prevented allograftspecific IgG production. Strikingly, CD19 mAb treatment significantly reduced renal allograft rejection and abrogated allograftspecific IgG development, whereas CD20 mAb treatment did not. By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation of adoptively transferred alloantigen-specific CD4+ T cells, demonstrating that B cells can also negatively regulate allograft rejection. Thereby, B cells can either positively or negatively regulate allograft rejection depending on the nature of the allograft and the intensity of the rejection response. Moreover, CD19 mAb may represent a new approach for depleting both B cells and plasma cells to concomitantly impair T cell activation, inhibit the generation of new allograft-specific Abs, or reduce preexisting allograft-specific Ab levels in transplant patients.

UR - http://www.scopus.com/inward/record.url?scp=79951838633&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79951838633&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.1002983

DO - 10.4049/jimmunol.1002983

M3 - Article

C2 - 21248259

AN - SCOPUS:79951838633

VL - 186

SP - 2643

EP - 2654

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 4

ER -