In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity

Pedro Horna, Alex Cuenca, Fengdong Cheng, Jason Brayer, Hong Wei Wang, Ivan Borrello, Hyam Levitsky, Eduardo M. Sotomayor

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Bone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4 + T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.

Original languageEnglish (US)
Pages (from-to)2871-2878
Number of pages8
JournalBlood
Volume107
Issue number7
DOIs
StatePublished - Apr 1 2006
Externally publishedYes

Fingerprint

Cross-Priming
T-cells
B-Cell Lymphoma
Antigen-Presenting Cells
Immunity
Chemical activation
Cells
T-Lymphocytes
Bone
Bone Marrow
Neoplasm Antigens
Antigens
B-Lymphocytes
CD4 Antigens

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity. / Horna, Pedro; Cuenca, Alex; Cheng, Fengdong; Brayer, Jason; Wang, Hong Wei; Borrello, Ivan; Levitsky, Hyam; Sotomayor, Eduardo M.

In: Blood, Vol. 107, No. 7, 01.04.2006, p. 2871-2878.

Research output: Contribution to journalArticle

Horna, Pedro ; Cuenca, Alex ; Cheng, Fengdong ; Brayer, Jason ; Wang, Hong Wei ; Borrello, Ivan ; Levitsky, Hyam ; Sotomayor, Eduardo M. / In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity. In: Blood. 2006 ; Vol. 107, No. 7. pp. 2871-2878.
@article{8d5ec7edd85d4b0aa282fdedebe0bc6a,
title = "In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity",
abstract = "Bone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4 + T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.",
author = "Pedro Horna and Alex Cuenca and Fengdong Cheng and Jason Brayer and Wang, {Hong Wei} and Ivan Borrello and Hyam Levitsky and Sotomayor, {Eduardo M.}",
year = "2006",
month = "4",
day = "1",
doi = "10.1182/blood-2005-07-3014",
language = "English (US)",
volume = "107",
pages = "2871--2878",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "7",

}

TY - JOUR

T1 - In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity

AU - Horna, Pedro

AU - Cuenca, Alex

AU - Cheng, Fengdong

AU - Brayer, Jason

AU - Wang, Hong Wei

AU - Borrello, Ivan

AU - Levitsky, Hyam

AU - Sotomayor, Eduardo M.

PY - 2006/4/1

Y1 - 2006/4/1

N2 - Bone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4 + T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.

AB - Bone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4 + T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.

UR - http://www.scopus.com/inward/record.url?scp=33645500590&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645500590&partnerID=8YFLogxK

U2 - 10.1182/blood-2005-07-3014

DO - 10.1182/blood-2005-07-3014

M3 - Article

C2 - 16339406

AN - SCOPUS:33645500590

VL - 107

SP - 2871

EP - 2878

JO - Blood

JF - Blood

SN - 0006-4971

IS - 7

ER -