Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Reactive astrocytes upregulate one or more gene products that are recognized by monoclonal antibody H


We generated a panel of monoclonal antibodies (mAbs) selected to recognize components from a Triton X-100 extract of ovine oligodendrocytes. One of these Abs, mAb H, recognizes an O-linked N-acetyl glucosamine residue in a specific conformation and/or environment. mAb H stained, weakly, two bands with M r×10–3 of 209 and 62 in lysates of cultured rat astrocytes, suggesting antigens of low abundance. We have employed immunohistochemistry to investigate the cell and tissue distribution of the mAb H antigen(s). In normal rat and human brains, the sparse reaction products detected were confined, mostly, to fibrous astrocytes. In sharp contrast, when pathological specimens from a variety of brain lesions, including anisomorphic and isomorphic gliosis, were examined, a strong reaction with mAb H was in evidence in all reactive astrocytes, independent of the origin or nature of the lesions. This we interpret as meaning that the gene product(s) recognized by this mAb is (are) upregulated or induced following injury to the brain. Hence, epitope H represents a new addition to the list of molecules that are affected by brain injury. Structural and functional identification of the antigen(s) should shed light on its (their) relevance to the pathophysiology of the disease process.

This is a preview of subscription content, log in to check access.

Author information

Additional information

Electronic Publication

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Arvanitis, D., Stavridou, A., Mori de Moro, G. et al. Reactive astrocytes upregulate one or more gene products that are recognized by monoclonal antibody H. Cell Tissue Res 304, 11–19 (2001).

Download citation

  • Brain injury Astrocytosis Glial cells Lesion-induced gene activation Monoclonal antibodies Gliosis Human Rat