ECTRIMS eLearning

CD44 as a trigger for inflammatory lesion formation
ECTRIMS Learn. Hochstrasser T. 10/27/17; 200618; P963
Tanja Hochstrasser
Tanja Hochstrasser
Contributions
Abstract

Abstract: P963

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models

During brain inflammation, immune cells first have to cross the endothelial barrier to gain access into the perivascular space, and second break through the glia limitans. This second step is poorly understood. CD44 is expressed by immune, as well as cells of the luminal and adluminal site. Thus, CD44 interaction might play a role during immune cell progression. In this project, we aim to investigate the relevance of CD44 for immune cell recruitment.
Activation of microglia and astrocytes was induced by cuprizone intoxication. Encephalitogenic immune cells in the peripheral lymphoid organs were induced by active immunization with the myelin protein peptide MOG35-55 (i.e. experimental autoimmune encephalomyelitis (EAE)). The liaison of innate and adaptive immunity was realized by combining the cuprizone model with active EAE (i.e. Cup/EAE). CX3CR1+/eGFP CCR2+/RFP transgenic mice were used to label microglia and monocytes.
In cuprizone-treated mice, CD44 was strongly induced at adluminal sites. The observed staining pattern suggested either expression of CD44 at the most distal astrocyte processes and/or secreted soluble CD44 in the extracellular space. To test, whether this brain intrinsic CD44 expression triggers peripheral immune cell recruitment into the brain, both models were combined. The liaison of innate and adaptive immunity resulted in massive recruitment of peripheral immune cells. Now, CD44 was expressed at the luminal and adluminal site. Detailed phenotypic characterization revealed that CD44 is expressed by both, CD3+ lymphocytes and RFP+ monocytes.
Our results suggest that CD44 is especially important for the progression of immune cells over the perivascular glia limitans.
Disclosure: Tanja Hochstrasser: nothing to disclose
Christin Rebecca Reinbach: nothing to disclose
Nicolas Pröbstl: nothing to disclose
Markus Kipp: nothing to disclose

Abstract: P963

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models

During brain inflammation, immune cells first have to cross the endothelial barrier to gain access into the perivascular space, and second break through the glia limitans. This second step is poorly understood. CD44 is expressed by immune, as well as cells of the luminal and adluminal site. Thus, CD44 interaction might play a role during immune cell progression. In this project, we aim to investigate the relevance of CD44 for immune cell recruitment.
Activation of microglia and astrocytes was induced by cuprizone intoxication. Encephalitogenic immune cells in the peripheral lymphoid organs were induced by active immunization with the myelin protein peptide MOG35-55 (i.e. experimental autoimmune encephalomyelitis (EAE)). The liaison of innate and adaptive immunity was realized by combining the cuprizone model with active EAE (i.e. Cup/EAE). CX3CR1+/eGFP CCR2+/RFP transgenic mice were used to label microglia and monocytes.
In cuprizone-treated mice, CD44 was strongly induced at adluminal sites. The observed staining pattern suggested either expression of CD44 at the most distal astrocyte processes and/or secreted soluble CD44 in the extracellular space. To test, whether this brain intrinsic CD44 expression triggers peripheral immune cell recruitment into the brain, both models were combined. The liaison of innate and adaptive immunity resulted in massive recruitment of peripheral immune cells. Now, CD44 was expressed at the luminal and adluminal site. Detailed phenotypic characterization revealed that CD44 is expressed by both, CD3+ lymphocytes and RFP+ monocytes.
Our results suggest that CD44 is especially important for the progression of immune cells over the perivascular glia limitans.
Disclosure: Tanja Hochstrasser: nothing to disclose
Christin Rebecca Reinbach: nothing to disclose
Nicolas Pröbstl: nothing to disclose
Markus Kipp: nothing to disclose

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies