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Oncolytic herpes simplex virus propagates tertiary lymphoid structure formation via CXCL10/CXCR3 to boost antitumor

Meng-Jie Zhang1, Wen-Ping Lin1, Qing Wang1

  • 1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.

Cell Proliferation
|September 2, 2024
PubMed

Insights

Oncolytic herpes simplex virus-1 (oHSV) promotes tertiary lymphoid structure (TLS) formation by recruiting stem-like CD8+ T cells via the CXCL10/CXCR3 pathway. This oHSV-induced TLS formation enhances antitumor immunity and improves responses to immunotherapy.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Tertiary lymphoid structures (TLS) are crucial for antitumor immunity.
  • Oncolytic herpes simplex virus-1 (oHSV) shows promise in cancer treatment, but its role in TLS formation is unclear.

Purpose of the Study:

  • To investigate the role of oHSV in TLS formation within tumor models.
  • To elucidate the mechanisms by which oHSV influences TLS and antitumor immunity.

Main Methods:

  • Utilized 4MOSC1 and MC38 subcutaneous tumor mouse models.
  • Administered oHSV and analyzed TLS formation, immune cell infiltration (B cells, TCF1+CD8+ T cells), and chemokine expression (CXCL10/CXCR3).
  • Investigated the impact of CXCL10/CXCR3 inhibition on T cells and granzyme B expression, and assessed combination therapy with αPD-1.

Main Results:

  • oHSV induced TLS formation and increased infiltration of B cells and stem-like TCF1+CD8+ T cells.
  • oHSV upregulated TLS-related chemokines, notably CXCL10/CXCR3, facilitating TLS.
  • CXCL10/CXCR3 pathway is essential for oHSV-mediated TLS formation and T cell proliferation; inhibition impaired these effects.
  • Combination of oHSV-mediated TLS formation with αPD-1 treatment improved anti-tumor response and survival rates.

Conclusions:

  • oHSV promotes TLS formation by recruiting stem-like TCF1+CD8+ T cells through the CXCL10/CXCR3 pathway.
  • oHSV-induced TLS formation enhances antitumor immunity and holds potential for combination therapies, particularly with αPD-1.
  • CXCL10 and CXCR3 are identified as key players in oHSV-driven anti-tumor immune responses and favorable prognostic factors in cancer patients.

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