Literature DB >> 27141363

IL-2/anti-IL-2 mAb immunocomplexes: A renascence of IL-2 in cancer immunotherapy?

Jakub Tomala1, Marek Kovar1.   

Abstract

The in vivo biological activity of IL-2 can be dramatically increased by complexing with anti-IL-2 mAb. Moreover, IL-2/anti-IL-2 mAb immunocomplexes selectively stimulate different subsets of immune cells, depending on the clone of anti-IL-2 mAb that is used. Thus, IL-2/S4B6 mAb complexes strongly stimulate CD122high populations, namely NK and memory CD8+ T cells. They also intermediately stimulate Treg cells. Conversely, IL-2/JES6.1 mAb immunocomplexes have no stimulatory activity for CD122high populations. However, they potently and highly selectively stimulate CD25+ cells (i.e., Treg and activated T cells). IL-2/S4B6 mAb immunocomplexes have also been shown to possess antitumor activity in various mouse tumor models.

Entities:  

Keywords:  Anti-IL-2 mAb; IL-2; cancer immunotherapy; immunocomplexes; selective stimulatory activity

Year:  2015        PMID: 27141363      PMCID: PMC4839359          DOI: 10.1080/2162402X.2015.1102829

Source DB:  PubMed          Journal:  Oncoimmunology        ISSN: 2162-4011            Impact factor:   8.110


  83 in total

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6.  Selective stimulation of T cell subsets with antibody-cytokine immune complexes.

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9.  In vivo expansion of activated naive CD8+ T cells and NK cells driven by complexes of IL-2 and anti-IL-2 monoclonal antibody as novel approach of cancer immunotherapy.

Authors:  Jakub Tomala; Helena Chmelova; Tomas Mrkvan; Blanka Rihova; Marek Kovar
Journal:  J Immunol       Date:  2009-10-15       Impact factor: 5.422

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Review 6.  Interleukin-6 at the Host-Tumor Interface: STAT3 in Biomolecular Condensates in Cancer Cells.

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7.  Influence of Different Age Cutoff Points on the Prediction of Prognosis of Cancer Patients Receiving ICIs and Potential Mechanistic Exploration.

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Review 8.  Next generation of immune checkpoint therapy in cancer: new developments and challenges.

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9.  Polymicrobial sepsis influences NK-cell-mediated immunity by diminishing NK-cell-intrinsic receptor-mediated effector responses to viral ligands or infections.

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