File:Cells-10-02800-g002-550.webp

English: Figure 2. Pathogenetic mechanisms of neutropenia. (A) Humoral abnormalities include anti-neutrophil antibodies and the release of soluble FasL, TNF-α and ΙFN-γ by leukemic cells. Fas–FasL interaction triggers neutrophils apoptosis. TNF-α and ΙFN-γ, instead, are supposed to promote Fas expression on BM myeloid progenitors. (B) BM infiltration by leukemic LGL or BM substitution, due to an excessive collagen deposition by MSC, might lead to an impaired granulopoiesis. (C) The expression of peculiar TCR/KIR on leukemic cells surface might be responsible of a cell-mediated cytotoxicity against neutrophils. BM: Bone marrow; HLA: human leukocyte antigens; ΙFN-γ: interferon-γ; KIR: killer immunoglobulin-like receptors; LGL: large granular lymphocytes; MSC: mesenchymal stromal cells; s-FasL: soluble Fas ligand; TCR: T-cell receptor; TNF-α: tumor necrosis factor α.