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Regulating the regulators via targeting CD38 in the tumor microenvironment.

Navnita Dutta1, Nabanita Halder2, Eduardo Nunes Chini3

  • 1Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, United States.

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|February 19, 2026
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CD38 drives immunosuppression in the tumor microenvironment by altering T cell metabolism and promoting regulatory cell survival. Targeting CD38 can reverse immune suppression and enhance cancer immunotherapy effectiveness.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Metabolic Regulation

Background:

  • The tumor microenvironment (TME) suppresses anti-cancer immunity.
  • CD38 is a key molecule expressed on various immune cells within the TME.
  • CD38's role in immune suppression and T cell function is under investigation.

Purpose of the Study:

  • To elucidate the multifaceted roles of CD38 in regulating the immunosuppressive TME.
  • To investigate CD38's impact on immune cell metabolism and function.
  • To evaluate CD38 as a therapeutic target for cancer immunotherapy.

Main Methods:

  • Analysis of CD38 expression on various immune cells in the TME.
  • Investigation of CD38's enzymatic activity and its downstream signaling pathways (NAD+ hydrolysis, calcium signaling).
  • Assessment of CD38's role in T cell metabolism (glycolysis, FAO, mitochondrial function) under hypoxic conditions.
  • Evaluation of therapeutic strategies targeting CD38 in preclinical models.

Main Results:

  • CD38 is highly expressed on immunosuppressive cells (Tregs, Bregs, MDSCs, TAMs, TANs), enhancing their survival and function.
  • CD38 depletes NAD+ in effector T cells, impairing their glycolysis and mitochondrial fitness, while promoting regulatory cell fatty acid oxidation (FAO).
  • CD38 signaling, via cADPR and NAADP, mobilizes calcium fluxes that reinforce immune suppression.
  • CD38 integrates with hypoxia-induced pathways in Bregs, promoting angiogenesis and therapeutic resistance.
  • Targeting CD38 reverses immune suppression, restores effector T cell activity, and improves tumor response to immunotherapy.

Conclusions:

  • CD38 acts as a critical metabolic regulator and immunologic checkpoint within the TME.
  • CD38 orchestrates suppressive immune networks and influences invariant natural killer T (iNKT) cell fate.
  • CD38 represents a promising therapeutic target for overcoming immune suppression and enhancing cancer immunotherapy.