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Bone chimera studies have shown, however, that in cases of extreme infection the blood–brain barrier will weaken, and microglia will be replaced with haematogenous, marrow-derived cells, namely myeloid progenitor cells and macrophages. Once the infection has decreased the disconnect between peripheral and central systems is reestablished and ...
Tumor-associated macrophages are mainly of the M2 phenotype, and seem to actively promote tumor growth. [56] Macrophages exist in a variety of phenotypes which are determined by the role they play in wound maturation. Phenotypes can be predominantly separated into two major categories; M1 and M2.
Tumor-associated macrophages/microglia are the main infiltrate in gliomas, comprising up to 40% of the tumor mass. [22] TAMs are either of peripheral origin (macrophages) or representing brain-intrinsic, yolk sac-derived microglia, that create a supportive stroma for neoplastic cell expansion and invasion. [21]
Melanie Greter is a Swiss neuroimmunologist and a Swiss National Science Foundation Professor in the Institute of Experimental Immunology at the University of Zurich.Greter explores the ontogeny and function of microglia and border-associated macrophages of the central nervous system to understand how they maintain homeostasis and contribute to brain-related diseases.
In a healthy brain, microglia direct the immune response to brain damage and play an important role in the inflammation that accompanies the damage. Many diseases and disorders are associated with deficient microglia, such as Alzheimer's disease , Parkinson's disease and ALS .
High expression of TREM2 was associated with shorter survival times of patients with ovarian cancer, gastric cancer, lower-grade glioma, hepatocellular carcinoma, or renal clear cell carcinoma. [50] Tumor infiltration by TREM2 +, APOE +, C1q + macrophage was reported to be a biomarker for recurrence of clear-cell renal carcinoma.
A decreased population of M2 macrophages and an increased population of M1 macrophages is associated with chronic inflammation. [19] Short-term inflammation is important in clearing cell debris from the site of injury, but it is this chronic, long-term inflammation that will lead to further cell death and damage radiating from the site of ...
Thus, CSF1R signaling in TAMs is associated tumor survival, angiogenesis, therapy resistance, and metastasis. Production of CSF-1 by brain tumors called glioblastomas causes microglia (brain-resident macrophages) to exhibit immunosuppressive, tumor-permissive phenotypes. [16]