ReviewThe veterinary quarterly2026
Apoptosis inhibitor of macrophage (AIM/CD5L) as a potential immunomodulator in feline injection-site sarcoma: a hypothesis on tumor-macrophage interactions.
Review in The veterinary quarterly, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
AIM (apoptosis inhibitor of macrophage), also known as CD5L, is a macrophage-derived scavenger protein with broad immunomodulatory roles in mammals. Secreted by tissue macrophages, AIM circulates bound to IgM pentamers, which stabilize the protein in blood; free AIM is released during inflammation to influence immune signaling and cellular homeostasis. (Yang et al. 2023). In cats, AIM exhibits distinctive structural and biochemical properties, existing as both a three-domain (37 kDa) and a four-domain (45 kDa) variant generated through exon 3 duplication (Evangelista et al. 2025), and binding IgM approximately 1000-fold more tightly than murine AIM due to a species-specific positively charged cluster in its third SRCR domain (Miyazaki et al., 2018). These differences suggest feline AIM may function distinctly from human/mouse AIM. Feline injection-site sarcomas (FISS) arise in the context of chronic inflammation and frequently contain abundant tumor-associated macrophages (TAMs)associated with tumor aggressiveness and progression (Gomes et al., 2025). Given AIM's macrophage origin and its established roles in inflammatory regulation, autophagy signaling, and complement-mediated tumor targeting, we propose a directional hypothesis: that the high-affinity IgM-binding of feline AIM constrains free AIM availability in vivo, shifting the functional balance away from complement-mediated tumor cytotoxicity and toward macrophage-intrinsic M2-polarizing pathways, thereby promoting an immunosuppressive tumor microenvironment that contributes to FISS progression. Exploring AIM in this context may provide new perspectives for investigation in feline tumor immunology.
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