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<p>The expression patterns of T and B cell activation genes, along with Immunoglobulin G (IgG) subclasses, offer key insights into breast cancer progression. This study examined expression changes in four breast cancer subtypes&#xa0;-&#xa0;Luminal B HER2+, Luminal B HER2−, Luminal-like, and Triple Negative Breast Cancer (TNBC)&#xa0;-&#xa0;compared to healthy controls. Serum IgG subclass concentrations were also evaluated across these subtypes. Using the RT<sup>2</sup> Profiler QPCR array, expression of 84 genes was assessed, revealing 39 upregulated and 7 downregulated genes in Luminal B HER2+, 33 and 11 in Luminal B HER2−, 47 and 15 in Luminal-like, and 36 and 12 in TNBC, respectively. Four genes involved in antibody production were commonly altered across all subtypes. CD27 (<i>P</i> = 0.0122) showed fold changes of 5.60, 87.39, 49.93, and 109.38, while CD28 (<i>P</i> = 0.0014) increased by 54.13, 15.54, 26.95, and 54.41-fold. CD40 (<i>P</i> = 0.0003) was upregulated with 31.88, 15.28, 23.82, and 19.25 folds across subtypes, as was IL7 (<i>P</i> = 0.0002), with 2.89, 2.84, 3.52 and 3.28-fold increase. Conversely, LAG3 (<i>P</i> = 0.0347) was consistently downregulated (fold changes: 0.01, 0.01, 0.04 and 0.45). Immune checkpoint analysis revealed significant upregulation of CD274 (<i>P</i> = 0.0045), CD47 (<i>P</i> = 0.0432), CD276 (<i>P</i> = 0.0310) and TLR9 (<i>P</i> = 0.0081), while LAG3 (<i>P</i> = 0.0347) were significantly downregulated. ELISA-based serum analysis showed significantly elevated IgG1 across all subtypes (<i>P</i> &lt; 0.007). IgG2 increased in Luminal B HER2− (<i>P</i> = 0.0007) and decreased in TNBC (<i>P</i> = 0.0004). IgG3 was reduced in Luminal B HER2+, Luminal-like, and TNBC (<i>P</i> &lt; 0.035), while IgG4 increased in Luminal B HER2+ and HER2− but decreased in TNBC. These findings highlight pronounced, subtype-specific adaptive and innate immune responses in breast cancer, reflecting the intricate landscape of immune modulation in tumorigenesis.</p>

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Expression profiling of T cell and B cell activation genes and immunoglobulin G subclasses in Egyptian breast cancer patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月19日

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  • Yara Elsherif,
  • Mona Rady,
  • Hesham Abdelaziz,
  • Mohamed El-Azizi

摘要

The expression patterns of T and B cell activation genes, along with Immunoglobulin G (IgG) subclasses, offer key insights into breast cancer progression. This study examined expression changes in four breast cancer subtypes - Luminal B HER2+, Luminal B HER2−, Luminal-like, and Triple Negative Breast Cancer (TNBC) - compared to healthy controls. Serum IgG subclass concentrations were also evaluated across these subtypes. Using the RT2 Profiler QPCR array, expression of 84 genes was assessed, revealing 39 upregulated and 7 downregulated genes in Luminal B HER2+, 33 and 11 in Luminal B HER2−, 47 and 15 in Luminal-like, and 36 and 12 in TNBC, respectively. Four genes involved in antibody production were commonly altered across all subtypes. CD27 (P = 0.0122) showed fold changes of 5.60, 87.39, 49.93, and 109.38, while CD28 (P = 0.0014) increased by 54.13, 15.54, 26.95, and 54.41-fold. CD40 (P = 0.0003) was upregulated with 31.88, 15.28, 23.82, and 19.25 folds across subtypes, as was IL7 (P = 0.0002), with 2.89, 2.84, 3.52 and 3.28-fold increase. Conversely, LAG3 (P = 0.0347) was consistently downregulated (fold changes: 0.01, 0.01, 0.04 and 0.45). Immune checkpoint analysis revealed significant upregulation of CD274 (P = 0.0045), CD47 (P = 0.0432), CD276 (P = 0.0310) and TLR9 (P = 0.0081), while LAG3 (P = 0.0347) were significantly downregulated. ELISA-based serum analysis showed significantly elevated IgG1 across all subtypes (P < 0.007). IgG2 increased in Luminal B HER2− (P = 0.0007) and decreased in TNBC (P = 0.0004). IgG3 was reduced in Luminal B HER2+, Luminal-like, and TNBC (P < 0.035), while IgG4 increased in Luminal B HER2+ and HER2− but decreased in TNBC. These findings highlight pronounced, subtype-specific adaptive and innate immune responses in breast cancer, reflecting the intricate landscape of immune modulation in tumorigenesis.