In-vivo generation of leukaemia-derived dendritic cells

Kolb, Hans‐Jochem; Rank, Andreas; Chen, Xiao; Woiciechowsky, Anja; Roskrow, Marie; Schmid, Christoph; Tischer, Johanna; Ledderose, Georg

doi:10.1016/j.beha.2004.06.004

Cited by 12 publications

(12 citation statements)

References 33 publications

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“…The culture time 10 to 14 days could be reduced by bacterial lysate of Streptococcus pyogenes , even shorter with calcium ionophore and IL4. However, application in vivo was restricted to GM‐CSF …”

Section: Production Of Dendritic Cells Of Leukemia Originmentioning

confidence: 99%

Hematopoietic stem cell transplantation and cellular therapy

Kolb

2017

HLA

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Allogeneic stem cell transplantation is a form of immunotherapy that has increased the chances of survival for patients with relapsed leukemia and high risk leukemia in remission. The major obstacles are graft-vs-host disease (GVHD) involving vital organs and infections. A most efficacious prophylaxis of GVHD is by depleting of T cells from the graft. However, problems of T-depleted transplants are rejection, slow recovery of the immune system and high incidence of relapse of leukemia and myeloma. The major problem of allogeneic transplantation is the separation of a graft-vs-leukemia (GVL) effect from GVHD. This review will summarize the factors influencing GVHD, ways to exploit rapid advances in our knowledge of histocompatibility, chimerism and tolerance for fostering GVL over GVHD, and in particular the use of cellular therapies including donor lymphocyte infusions for disease control.

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Section: Production Of Dendritic Cells Of Leukemia Originmentioning

confidence: 99%

Hematopoietic stem cell transplantation and cellular therapy

Kolb

2017

HLA

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“…Salvage post-transplant maneuvers have focused on utilization of second transplants, but these are limited to a minority (10% in most series) of fit patients. Clinical and pre-clinical data has suggested a role for cytokine therapy in the induction of graft versus leukemia effects in the setting of post-transplant relapse (Slavin et al 1996; Cortes et al 1998; Boyer et al 2000; Mohty et al 2002; Kolb et al 2004; Li and Waller 2004). Improving the antigen-presenting capacity of leukemic blasts may lead to clinically-significant anti-leukemic effects.…”

Section: Gm-csf May Augment the Graft Versus Leukemia Effect Of Allogmentioning

confidence: 99%

Clinical uses of GM-CSF, a critical appraisal and update

Arellano

Lonial²

2008

BTT

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The role of granulocyte-macrophage-colony-stimulating factor (GM-CSF) in the supportive care of cancer patients has been evaluated with promising results. More recently, GM-CSF has been added to regimens for the mobilization of hematopoietic progenitor cells. An expanding role for GM-CSF in regulating immune responses has been recognized based upon its activity on the development and maturation of antigen presenting cells and its capability for skewing the immune system toward Th1-type responses. GM-CSF has been shown to preferentially enhance both the numbers and activity of type 1 dendritic cells (DC1), the subsets of dendritic cells responsible for initiating cytotoxic immune responses. The increase in DC1 content and activity following local and systemic GM-CSF administration support a role for GM-CSF as an immune stimulant and vaccine adjuvant in cancer patients. GM-CSF has shown clinical activity as an immune stimulant in tumor cell and dendritic cell vaccines, and may increase antibody-dependent cellular cytotoxicity. The successful use of myeloid acting cytokines to enhance anti-tumor responses will likely require the utilization of GM-CSF in combination with cytotoxic or other targeted therapies.

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“…Indeed, CML is different than almost any other cancer in that DC immunotherapy would not require the pulsing of DC with exogenous antigens, since CML DC endogenously express BCR-ABL immunogenic peptides at sufficient concentrations to stimulate a T cell response [80]. This concept has been demonstrated clinically through the use of GM-CSF administration to expand endogenous DC numbers followed by donor lymphocyte infusion, resulting in a positive impact on patient survival that was associated with increased anti-leukemic response [81], which was believed to be due to enhanced presentation of leukemic antigens from DC. However the treatment proposed here is less "invasive" and more applicable to widespread implementation.…”

Section: Aldara™ Stimulation Of Cml-specific Responsesmentioning

confidence: 99%

Therapeutic use of Aldara™ in chronic myeloid leukemia

Marleau¹,

Lipton

Riordan³

et al. 2007

J Transl Med

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The potent clinical responses seen in patients with chronic myeloid leukemia (CML) after administration of donor-specific lymphocytes, as well as the correlation between the presence of antigen specific T cells and prolonged remission in these patients, suggests a role for the immunological control of CML. Here we propose Aldara™, a clinically used formulation of imiquimod, as an agent for augmenting immune responses to CML antigens. Our proposition is based upon 3 tenets: 1) Endogenous dendritic cells (DC) of CML patients, which are known to be derived from the malignant clone, express and present various leukemic antigens; 2) CML-antigen reactive T cell clones exist in the patient but in many situations are ineffectively stimulated to cause significant hematological responses; and 3) Antigen presentation by mature, activated DC, which endogenously express CML-antigens may endow the pre-existing ineffective T cell responses with ability to control CML progression. The practical use of Aldara™ as a localized activator of DC in the context of present day leukemic therapeutics, as well as various properties of this unique immune modulator will be discussed.

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In-vivo generation of leukaemia-derived dendritic cells

Cited by 12 publications

References 33 publications

Hematopoietic stem cell transplantation and cellular therapy

Hematopoietic stem cell transplantation and cellular therapy

Clinical uses of GM-CSF, a critical appraisal and update

Therapeutic use of Aldara™ in chronic myeloid leukemia

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