CSF3R抗体—艾普蒂

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     The image is immunohistochemistry of paraffin-embedded Human brain tissue using P02445(CLU/APO J Antibody) at dilution 1/60. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human liver cancer tissue using P02445(CLU/APO J Antibody) at dilution 1/60. (Original magnification: ×200)    

  
  

The CSF3R antibody targets the colony-stimulating factor 3 receptor (CSF3R), a cell surface protein critical for neutrophil production and function. CSF3R, also known as the granulocyte colony-stimulating factor (G-CSF) receptor, is primarily expressed on myeloid progenitor cells and mature neutrophils. It activates downstream signaling pathways, including JAK-STAT and MAPK, upon binding to G-CSF, promoting neutrophil differentiation, survival, and mobilization.

In clinical contexts, CSF3R antibodies are associated with autoimmune disorders and hematologic malignancies. Autoantibodies against CSF3R are implicated in chronic neutropenia, where they disrupt G-CSF signaling, impairing neutrophil maturation. Conversely, somatic mutations in CSF3R (e.g., truncation variants) are linked to chronic neutrophilic leukemia (CNL) and atypical chronic myeloid leukemia (aCML), driving constitutive receptor activation and uncontrolled myeloid proliferation.

Diagnostically, CSF3R antibodies serve as biomarkers. In autoimmune neutropenia, their detection aids in differentiating immune-mediated causes from congenital or drug-induced forms. In oncology, CSF3R mutation screening guides classification and therapeutic decisions, as certain mutations predict sensitivity to JAK inhibitors. Research also explores therapeutic anti-CSF3R monoclonal antibodies to block aberrant signaling in malignancies or modulate neutrophil activity in inflammatory diseases. Overall, CSF3R antibodies hold dual significance as pathogenic agents and tools for diagnosis/treatment in hematologic and immune disorders.