Background: Two major ways of macrophage (MΦ) activation can occur in radiation-induced pulmonary injury (RPI): classical and alternative MΦ activation, which play important roles in the pathogenesis of RPI. MΦ can produce chemokine MΦ inflammatory protein-1α (MIP-1α), while MIP-1α can recruit MΦ. The difference in the chemotactic ability of MIP-1α toward distinct activated MΦ is unclear. We speculated that there has been important interaction of MIP-1α with different activated MΦ, which might contribute to the pathogenesis of RPI.Methods: Classically and alternatively activated MΦ were produced by stimulating murine MΦ cell line RAW 264.7 cells with three different stimuli (LPS, IL-4 and IL-13); Then we used recombinant MIP-1α to attract two types of activated MΦ. In addition, we measured the ability of two types of activated MΦ to produce MIP-1α at the protein or mRNA level.Results: Chemotactic ability of recombinant MIP-1α toward IL-13-treated MΦ was the strongest, was moderate for IL-4-treated MΦ, and was weakest for LPS-stimulated MΦ (p < 0.01). The ability of LPS-stimulated MΦ to secrete MIP-1α was significantly stronger than that of IL-4-treated or IL-13-treated MΦ (p < 0.01). The ability of LPS-stimulated MΦ to express MIP-1α mRNA also was stronger than that of IL-4- or IL-13-stimulated MΦ (p < 0.01).Conclusions: The chemotactic ability of MIP-1α toward alternatively activated MΦ (M2) was significantly greater than that for classically activated MΦ (M1). Meanwhile, both at the mRNA and protein level, the capacity of M1 to produce MIP-1α is better than that of M2. Thus, chemokine MIP-1α may play an important role in modulating the transition from radiation pneumonitis to pulmonary fibrosisin vivo, through the different chemotactic affinity for M1 and M2.

Background: Advanced pancreatic cancer carries a dismal prognosis. Current chemotherapy provides limited survival benefit while causing substantial toxicity. Despite numerous trials, combining gemcitabine with other cytotoxic or targeted agents has not significantly improved outcomes, highlighting the urgent need for novel therapeutic strategies.Case presentation: This report describes a 56-year-old male diagnosed with stage IVB pancreatic tail adenocarcinoma, characterized by a high tumor mutational burden (TMB-H) and a KRAS wild-type status. The patient showed a significant therapeutic response and an improved quality of life after receiving a novel four-drug combination regimen. The treatment included cadonilimab (a PD-1/CTLA-4 bispecific antibody), nimotuzumab (an EGFR monoclonal antibody), albumin-bound paclitaxel, and gemcitabine. After two cycles, the primary pancreatic lesion reduced by 37%, and there was substantial shrinkage of hepatic metastases. Continued treatment maintained partial remission (PR), with progression-free survival (PFS) lasting over seven months and manageable toxicity.Conclusion: This case highlights the potential of the combination of cadonilimab, nimotuzumab, albumin-bound paclitaxel, and gemcitabine as an effective, low-toxicity treatment option for patients with TMB-H/KRAS wild-type advanced pancreatic cancer.

Clear cell renal cell carcinoma (ccRCC) frequently resists targeted and immune therapies, necessitating predictive biomarkers. Thyroid hormone receptor bet