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CCL22 Signaling in the Tumor Environment

Natascha Röhrle1, Max M L Knott2, David Anz3,4

  • 1Center of Integrated Protein Science Munich (CIPS-M) and Division of Clinical Pharmacology, Klinikum der Ludwig-Maximilians-Universität München, Munich, Germany.

Advances in Experimental Medicine and Biology
|February 16, 2020
PubMed

Insights

Tumors suppress T cell immunity using regulatory T cells (T regs). The chemokine CCL22 recruits these T regs, hindering antitumor responses. Targeting the CCL22-CCR4 pathway may enhance cancer immunotherapy.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • T cell-mediated immunity is crucial for eliminating cancer cells.
  • Tumors employ regulatory mechanisms, including regulatory T cells (T regs), to evade immune detection.
  • The chemokine CCL22, produced by dendritic cells (DCs), is implicated in recruiting T regs via its receptor CCR4.

Purpose of the Study:

  • To review the role of CCL22 in cancer immunity.
  • To elucidate mechanisms of CCL22-mediated immune suppression.
  • To explore therapeutic strategies targeting the CCL22-CCR4 axis.

Main Methods:

  • Literature review of existing studies on CCL22 and cancer immunity.
  • Analysis of CCL22's role in T reg migration and DC-T reg interactions.
  • Discussion of factors influencing CCL22 expression and therapeutic targeting.

Main Results:

  • CCL22 promotes T reg accumulation in tumor tissues, suppressing antitumoral immunity.
  • CCL22 facilitates the formation of DC-T reg contacts in lymph nodes, further inhibiting immune responses.
  • The CCL22-CCR4 axis is a key regulator of T cell suppression in the tumor microenvironment.

Conclusions:

  • CCL22 plays a significant role in tumor immune evasion by recruiting and activating regulatory T cells.
  • Understanding CCL22's function provides insights into overcoming immune suppression in cancer.
  • Targeting the CCL22-CCR4 axis presents a promising therapeutic avenue for enhancing cancer immunotherapy.
Keywords:
Antitumor immunityCCL22CCR4ChemokinesDendritic cellsIL-1 αImmune checkpointImmune escapeImmunosuppressionImmunotherapyLymph nodeProstaglandin E2Regulatory T cellsT cell immunityTumor environment

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