Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2001 Feb;30(1):57-64.
doi: 10.1081/imm-100103691.

A quantitative analysis of CD45Rlow CD4+ T cells in the subarachnoid space of Lewis rats with autoimmune encephalomyelitis

Affiliations

A quantitative analysis of CD45Rlow CD4+ T cells in the subarachnoid space of Lewis rats with autoimmune encephalomyelitis

T Shin et al. Immunol Invest. 2001 Feb.

Abstract

In order to quantify encephalitogenic effector T cells in the subarachnoid space (SAS) and spinal cord afflicted with experimental autoimmune encephalomyelitis (EAE), we immunized Lewis rats using myelin basic protein and complete Freund's adjuvants and analyzed the inflammatory cells by fluorescence-activated cell sorter (FACS) and immunohistochemistry. At the induction stage of EAE, the majority of observed inflammatory cells were determined by immunohistochemistry to be either CD4+ T cells or OX42+ macrophages. Among CD4+ T cells, both CD45R high (OX22+) and CD45R low (OX22-) T cells were found in the SAS, while in the neighboring subpial spinal cord parenchyma, CD45R low (OX22-negative)/ CD4+ T cells predominated. FACS analysis showed that CD45RC low/CD4+ T cells was 83% of total CD4+ T cells in the SAS, while 94% of cells with the same phenotype were found in the parenchyma of rat spinal cords afflicted with EAE. This finding suggests that during the induction stage of EAE, effector T cells preferentially migrate into the subpial parenchyma from the SAS. Thereafter, suppressor T cells follow, which may lead to the spontaneous recovery from EAE paralysis.

PubMed Disclaimer

Publication types

MeSH terms

Substances

LinkOut - more resources