Regulatory role of CD19 molecules in B-cell activation and differentiation

Rie, Menno A. de; Schumacher, Ton N.; Schijndel, G. M. W. Van; Lier, René A. W. van; Miedema, Frank

doi:10.1016/0008-8749(89)90385-7

Cited by 54 publications

(36 citation statements)

References 47 publications

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“…First, Rappocciolo et al isolated CD19-expressing B cells by positive selection. We chose negative selection (Figures 1 and 2) or none at all (Figure 3-7) to minimize potential signaling events from CD19 ligation (55) that might, in turn, alter the phenotype of the cells prior to or after KSHV infection. Second, Rappocciolo et al used peripheral blood B cells preactivated for 36 hours by CD40L and IL-4 for most of their work, while we used exclusively tonsillar cells, omitting CD40L and IL4 pretreatment.…”

Section: Discussionmentioning

confidence: 99%

KSHV infects a subset of human tonsillar B cells, driving proliferation and plasmablast differentiation

Hassman

Ellison²,

Kedes³

2011

J. Clin. Invest.

102

112

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Section: Discussionmentioning

confidence: 99%

KSHV infects a subset of human tonsillar B cells, driving proliferation and plasmablast differentiation

Hassman

Ellison²,

Kedes³

2011

J. Clin. Invest.

102

112

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“…CD19 is involved in B-cell fate and differentiation through the modulation of B-cell receptor signaling at multiple stages of B-cell development (29,30). CD19 is ubiquitously expressed on B cells (25), as it is found expressed from the early pre-B stage throughout B-cell differentiation up to mature B cells, before it is downmodulated at the plasma cell stage (Fig.…”

Section: Cd19 Antigenmentioning

confidence: 99%

SAR3419: An Anti-CD19-Maytansinoid Immunoconjugate for the Treatment of B-Cell Malignancies

Blanc

Bousseau

Caron

et al. 2011

Clinical Cancer Research

149

118

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SAR3419 is a novel anti-CD19 humanized monoclonal antibody conjugated to a maytansine derivate through a cleavable linker for the treatment of B-cell malignancies. SAR3419 combines the strengths of a high-potency tubulin inhibitor and the exquisite B-cell selectivity of an anti-CD19 antibody. The internalization and processing of SAR3419, following its binding at the surface of CD19-positive human lymphoma cell lines and xenograft models, release active metabolites that trigger cell-cycle arrest and apoptosis, leading to cell death and tumor regression. SAR3419 has also been shown to be active in different lymphoma xenograft models, including aggressive diffuse large B-cell lymphoma, resulting in complete regressions and tumor-free survival. In these models, the activity of SAR3419 compared favorably with rituximab and lymphoma standard of care chemotherapy. Two phase I trials with 2 different schedules of SAR3419 as a single agent were conducted in refractory/relapsed B-cell non-Hodgkin lymphoma. Activity was reported in both schedules, in heavily pretreated patients of both follicular and diffuse large B-cell lymphoma subtypes, with a notable lack of significant hematological toxicity, validating SAR3419 as an effective antibody-drug conjugate and opening opportunities in the future. Numerous B-cell-specific anti-CD19 biologics are available to treat B-cell non-Hodgkin lymphoma, and early phase I results obtained with SAR3419 suggest that it is a promising candidate for further development in this disease. In addition, thanks to the broad expression of CD19, SAR3419 may provide treatment options for B-cell leukemias that are often CD20-negative.

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“…T h e following mAb were used: NKI-L15 (anti-LFA-la, C D lla , IgG2a), NKI-L7 (anti-LFA-la, C D lla, IgG l; [46]), NKI-L16 (anti-LFA-la^ C D lla activation epitope, IgG2a; [43]), NKI-P1 (anti-CD44, IgGl; [47]), SAM-1 (anti-VLA-5, CD49e, IgG2b, [48]), CLB-CD19 (anti-CD19, IgG2a; [49]), 1H4 (anti-CD20, IgGl), SPV-T3b (anti-CD3, IgG2a, [50]), CLB-T3/3 (anti-CD3, IgG2a; [30]), from R. van Lier, Amsterdam, CLB-LFA-1/1 (anti-LFA-lfl, CD18, IgGl; [51]), from F. Miedema, Amster dam , CLB-FcR-granl (anti-FcyRIII, CD 16, IgG2a; [52]), from P. Tetteroo, Amsterdam, GoH3 (anti-VLA-6, CD49f, rat IgG2a; [53]), from A. Sonnenberg, Amsterdam, 60,3 (anti-CD18, IgG2a; [25]), from M. Harlan, Seattle, Ts2/9 (anti-LFA-3, CD58, IgG l, [54]), fromT. Springer, Boston, M A , HP1/3 (anti-VLA-4cx, CD49d, IgGl; [55]), from E Sanchez-Madrid, Madrid, 4F2 (anti-4F2 activation anti gen, IgG2a; [56]), F10.2 (anti-ICAM-1, CD54, IgG l; [57]), …”

Section: Mabmentioning

confidence: 99%

Role of LFA‐1/ICAM‐1 in interleukin‐2‐stimulated lymphocyte proliferation

et al. 1993

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Major adhesion routes between lymphoid cells involve the receptor/ligand pairs LFA-l/ICAM-1 and CD2/LFA-3, in addition to VLA or CD44 molecules. In this study we evaluated the role of these adhesion receptors in the proliferative response of lymphoid cells to interleukin-2 (IL-2). Blocking studies were performed with a panel of monoclonal antibodies (mAb) directed against these adhesion molecules. Selective inhibition of recombinant (r)IL-2-induced cell proliferation was observed with mAb directed against the a or ¡3 subunit of LFA-1 or to its ligand ICAM-1. Interestingly, rIL-2-induced proliferation was also inhibited by NKI-L16, an anti-la antibody known to enhance cell-cell interac tion. Resting lymphocytes were preferentially susceptible to the inhibition, particularly in an early phase of culture and when stimulated with a relatively low dose of rIL-2. By using mAb that specifically could block distinct rIL-2 activation pathways, LFA-l/ICAM-1 interaction was found to be required for p55 IL-2 receptor (IL-2R)-mediated interaction of rIL-2 with its high-affinity receptor, but not for p75 IL-2R-rnediated responses. Furthermore, it was shown that the rIL-2 response of T lymphocytes, but not of natural killer cells, was dependent on LFA-l/ICAM-1 interaction. This suggests that LFA-l/ICAM-1 interaction is required for an optimal iiL-2 response of cells capable of IL-2 secretion. Our data provide evidence for the hypothesis that adhesion receptor-directed release of IL-2 may result in a locally high concentration of IL-2 that triggers high-affinity IL-2R signaling and up-regulates p55 IL-2R to enhance cytokine responsive ness.

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Regulatory role of CD19 molecules in B-cell activation and differentiation

Cited by 54 publications

References 47 publications

KSHV infects a subset of human tonsillar B cells, driving proliferation and plasmablast differentiation

KSHV infects a subset of human tonsillar B cells, driving proliferation and plasmablast differentiation

SAR3419: An Anti-CD19-Maytansinoid Immunoconjugate for the Treatment of B-Cell Malignancies

Role of LFA‐1/ICAM‐1 in interleukin‐2‐stimulated lymphocyte proliferation

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