Anti-CCL5 polyclonal antibody [Biotin]

Background: Lysosomal storage diseases (LSD) are a large family of inherited disorders characterized by abnormal endolysosomal accumulation of cellular material due to catabolic enzyme and transporter deficiencies. Depending on the affected metabolic pathway, LSD manifest with somatic or central nervous system (CNS) signs and symptoms. Neuroinflammation is a hallmark feature of LSD with CNS involvement such as mucolipidosis type IV, but not of others like Fabry disease. Methods: We investigated the properties of microglia from LSD with and without major CNS involvement in 2-month-old mucolipidosis type IV (Mcoln1(-/-)) and Fabry disease (Gla(y/-)) mice, respectively, by using a combination of flow cytometric, RNA sequencing, biochemical, in vitro and immunofluorescence analyses. Results: We characterized microglia activation and transcriptome from mucolipidosis type IV and Fabry disease mice to determine if impaired lysosomal function is sufficient to prime these brain-resident immune cells. Consistent with the neurological pathology observed in mucolipidosis type IV, Mcoln1(-/-) microglia demonstrated an activation profile with a mixed neuroprotective/neurotoxic expression pattern similar to the one we previously observed in Niemann-Pick disease, type C1, another LSD with significant CNS involvement. In contrast, the Fabry disease microglia transcriptome revealed minimal alterations, consistent with the relative lack of CNS symptoms in this disease. The changes observed in Mcoln1(-/-) microglia showed significant overlap with alterations previously reported for other common neuroinflammatory disorders including Alzheimer's, Parkinson's, and Huntington's diseases. Indeed, our comparison of microglia transcriptomes from Alzheimer's disease, amyotrophic lateral sclerosis, Niemann-Pick disease, type C1 and mucolipidosis type IV mouse models showed an enrichment in "disease-associated microglia" pattern among these diseases. Conclusions: The similarities in microglial transcriptomes and features of neuroinflammation and microglial activation in rare monogenic disorders where the primary metabolic disturbance is known may provide novel insights into the immunopathogenesis of other more common neuroinflammatory disorders.

Purpose: To screen novel candidate biomarkers in primary colorectal cancer (CRC), and indentify their clinical valuation in progress of colorectal cancer. Methods: By using antibody microarray, 274 target proteins in tissue samples from primary colorectal cancer patients were detected. Among differently expressed proteins in CRC tissues, As promising candidate biomarker, RANTES/CCL5 was validated by enzyme-linked immunosorbentassay and immunohistochemistry (IHC), and the clinical significance of CCL5 was analyzed. Results: Totally, 25 differentially expressed proteins were indentified between colorectal cancers and matched normal mucosa. CCL5 expression was significantly associated with adverse pathological progress, apt to lymph node metastasis and higher T stage. Conclusions: CCL5 may contribute to promoting tumor growth, and CCL5 is a promising target that may help in understanding the pathogenesis of CRC.