作者: Vincenzo Bronte , Elisa Apolloni , Anna Cabrelle , Roberto Ronca , Paolo Serafini
DOI: 10.1182/BLOOD.V96.12.3838
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摘要: Apoptotic death of CD8(+) T cells can be induced by a population inhibitory myeloid that are double positive for the CD11b and Gr-1 markers. These responsible immunosuppression observed in pathologies as dissimilar tumor growth overwhelming infections, or after immunization with viruses. The appearance CD11b(+)/Gr-1(+) macrophages (iMacs) could attributed to high levels granulocyte-macrophage colony-stimulating factor (GM-CSF) vivo. Deletion iMacs vitro vivo reversed depression T-cell function. We isolated from spleens immunocompromised mice found these were CD31, ER-MP20 (Ly-6C), ER-MP58, markers characteristic granulocyte/monocyte precursors. Importantly, although retained their properties when cultured standard medium, suppressive functions modulated cytokine exposure. Whereas culture interleukin 4 (IL-4) increased iMac activity, differentiated into nonadherent fully mature highly activated dendritic presence IL-4 GM-CSF. A common CD31(+)/CD11b(+)/Gr-1(+) progenitor thus give rise capable either activating inhibiting function lymphocytes, depending on milieu prevails during antigen-presenting cell maturation. (Blood. 2000;96:3838-3846)