Summary: TEHRAN (FNA)- Cancerous tumors trick
myeloid cells, an important part of the immune system, into perceiving them as a damaged part of the body; the tumors actually put
myeloid cells to work helping them grow and metastasize (spread).
The lack of responsiveness of fibroblasts to TRAIL might be due to the lack of TRAIL ligand (as a consequence of decreased expression and/or
myeloid cell recruitment into the lungs, as revealed by decreased CD33 cells), internalization of the TRAIL receptors, and increased presence of IL13 or other intrinsic differences between IPF and normal lung fibroblasts.
Waer, "Transient expansion of [Mac1.sup.+]Ly6-[G.sup.+]Ly6-[C.sup.+] early
myeloid cells with suppressor activity in spleens of murine radiation marrow chimeras: possible implications for the graft-versus-host and graft-versus-leukemia reactivity of donor lymphocyte infusions," Blood, vol.
During tumor development,
myeloid cells accumulate massively within the tumor and regulate inflammatory and immune responses [74].
Therefore, a high index of suspicion and recognition of immature
myeloid cells associated with the reactive cells are required to establish the diagnosis of myeloid sarcoma.
The CCAAT enhancer binding proteins (C/EBPs) are a family of basic leucine zipper transcription factors which participate in the differentiation of several cell types including
myeloid cells (Morosetti et al.
We specifically examined the cytotoxic effects of BT on a human
myeloid cell line, a class of cells from the organ mainly affected by benzene.
This t(9;22) translocation results in the formation of the BCR-ABL fusion gene, which codes for a novel protein tyrosine kinase (TK) that is constitutively activated and therefore leads to increased proliferation of
myeloid cells, decreased apoptosis and adhesion, and genetic instability of the leukaemic cells.
The most predominant feature of CML is severe leukocytosis with the entire spectrum of
myeloid cell development appearing in the peripheral blood.
Subsequent chapters address the identification of novel
myeloid cell surface receptors, identifying novel ligands, phagocytosis, genetic manipulation, macrophage activation, lipid signaling, and the secretion of matrix metalloproteinases by macrophages.
These clinical conditions are characterized by high
myeloid cell mass and turnover associated with maturation (21, 22).
Researchers and practitioners in a wide range of medical specialties mark a century of
myeloid cell immunobiology by taking stock of past developments, reviewing current knowledge, and identifying future needs.
