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Table 1 CAF subtypes review

From: Metabolic and immune crosstalk between cancer-associated fibroblasts and pancreatic cancer cells

CAF subtype

Regulatory factors

Functional roles in tumor progression

References

Myofibroblastic CAF (myCAF)

TGF-β, ARP2/3, FAK, mechanical stress, FKBP7​

ECM deposition, increased stiffness, immune exclusion, supports tumor growth

[40,41,42,43,44,45,46,47]

Inflammatory CAF (iCAF)

IL-1/JAK-STAT pathway, IL-6, mTOR signaling​

Secretion of cytokines (IL-6, CXCL12), enhances invasion, immune suppression

[12, 15, 27, 48]

Antigen-presenting CAF (apCAF)

IL-1, TGF-β, mesothelial transition​

Antigen presentation without co-stimulation; induces CD4⁺ T cell anergy or Treg differentiation

[49,50,51,52]

Senescent CAF

Cellular senescence, SASP phenotype, PLAU​

Strongly immunosuppressive, limits CD8⁺ T cell infiltration

[110, 111]

LRRC15⁺ CAF

TGF-β-dependent​

Directly suppresses CD8⁺ T cells, associated with immunotherapy resistance

[49, 109]

CD105⁺ CAF

Adaptive immunity-dependent signals​

Supports tumor growth; CD105⁻ CAF Anti-tumor effects

[99, 116]

Endothelial-like CAF (endoCAF)

VEGF, CD144-β-catenin-STAT3 axis​

Vascular mimicry, enhances tumor metastasis through paracrine signaling

[38, 39]

Restraining CAF (rCAF)

Meflin​

Anti-tumor activity, inhibits tumor progression

[56]

MAPK-high CAF (mapCAF)

MAPK signaling, TGF-β, hypoxia response​

Reduced basal-like tumor cells and CD8⁺ T cells infiltration, immunoregulatory

[57]

FAPα⁺CD144⁺ endoCAF

CD144-β-catenin-STAT3 signaling axis​

Promotes metastasis, supports vascular mimicry, tumor invasion

[58]

  1. These CAF subtypes are classified from different perspectives and are not mutually exclusive, exhibiting substantial overlap