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      HomeProduct ApplicationThe Great Reveal of 'Undercover Agents' Inside Tumors: Who is the Ace Killer Among NK, T, and B Cells in Cancer Fight?

      The Great Reveal of 'Undercover Agents' Inside Tumors: Who is the Ace Killer Among NK, T, and B Cells in Cancer Fight?

      The tumor microenvironment (TME) is a battleground where immune cells and cancer cells vie against each other. The infiltration capabilities and functional differences of NK cells, T cells, and B cells determine the success or failure of anti-tumor immunity. This article will compare and contrast the mechanisms of infiltration, characteristics of action, and clinical significance of these three types of cells, taking you through the mysteries of this "immune tug-of-war"!

      1. NK Cells: The "Rapid Response Force" in the Early Stages of Tumors

      NK cells are core members of the innate immune system, capable of identifying and killing abnormal cells without prior antigen sensitization. Research has found that NK cells can infiltrate the lesion site in the early stages of tumors and directly kill cancer cells by releasing perforin and granzymes. Their infiltration ability is closely related to the CXCR3/CXCL9-11 chemokine axis. For example, in melanoma, renal cancer, and lung cancer, the degree of NK cell infiltration is positively correlated with patient survival rates.
      However, the tumor microenvironment can weaken the activity of NK cells by secreting inhibitory factors such as TGF-β. Additionally, changes in the expression of NK cell receptors (such as NKG2D, NKp30) also affect their function. For instance, abnormalities in the NKp30/B7-H6 axis in neuroblastoma are associated with poor prognosis.

       

      2. T Cells: The "Main Force" for Precision Strikes

      CD8+ T cells are the "stars" of anti-tumor immunity, activated after dendritic cells (DCs) present tumor antigens, and are chemoattracted to the core area of the tumor through the CXCR3 receptor. A high tumor mutational burden (TMB) can enhance their infiltration and directly kill cancer cells by secreting IFN-γ. In colorectal cancer models, co-infiltration of CD8+ T cells and NK cells can synergistically destroy tumor spheres.

      CD4+ T cells exhibit functional differentiation:

      Th1 cells activate CD8+ T cells through IFN-γ, enhancing the anti-tumor response;
      Treg cells secrete IL-10, TGF-β to suppress immune responses and are often enriched at the tumor edge. It is important to note that T cells are prone to exhaustion, characterized by the upregulation of immune checkpoint molecules such as PD-1, CTLA-4.

      3. B Cells: The "Regulator" with Dual Roles

      The infiltration and function of B cells are the most controversial, with their roles highly dependent on tumor types and microenvironments:

      Anti-tumor potential: In breast cancer and ovarian cancer, B cells co-infiltrate with T cells into tertiary lymphoid structures (TLS), enhancing the immune response by presenting antigens or secreting antibodies. Patients with high CD20+ B cell infiltration in triple-negative breast cancer have better prognoses.
      Pro-tumor characteristics: In gastric cancer, tumor-derived B cells significantly inhibit T cell proliferation (Ki-67 expression decreased from 13.9% to 5.1%), possibly involving the upregulation of PD-L1 or the secretion of IL-10, TGF-β. In liver cancer, B cells even mediate immune evasion through IgG.

      Comparative Summary: The Triangular Relationship of Synergy and Balance

      Cell Type Infiltration Characteristics Core Function Clinical Significance
      NK Cells Early rapid infiltration, rely on chemokines Direct killing, inhibited by TGF-β Positively correlated with prognosis, but easily suppressed by the microenvironment
      CD8+ T Cells High TMB promotes infiltration Precise killing, prone to exhaustion Key target for immunotherapy
      B Cells Associated with TLS formation Dual role: promote or suppress immunity Determines prognostic value based on tumor type

       

      Prospects: Regulating Infiltration, Optimizing Immunotherapy

      Current research suggests that combining targeting of NK cell activation receptors (such as NKG2D), reversing T cell exhaustion (such as PD-1 inhibitors), and modulating B cell functions (such as blocking IL-10) may become key to breaking through tumor immune suppression. Future efforts need to further elucidate the dynamic interactions among the three in different cancer types to provide new ideas for personalized therapy!

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      June 12, 2025

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