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Protein NFAT5, key for communication between macrophages and lymphocytes

A study published in Journal of Experimental Medicine has described a new mechanism that promotes antigen presentation by macrophages. 
18.10.2018

 

The team led by Cristina López-Rodríguez and Jose Aramburu, researchers at the Department of Experimental and Health Sciences (DCEXS) of Pompeu Fabra University, has described a new mechanism that promotes antigen presentation by macrophages

Macrophages are immune system cells that act as sensors within the tissues in which they are found. Thus, they regulate tissue integrity, both facilitating their functioning under normal conditions and when there is a disease. 

The researchers describe a new molecular mechanism that promotes antigen presentation by macrophages to T CD4 lymphocytes.

One of the functions of macrophages is to present the antigens that are found in the tissues - which are external substances that can trigger an immune reaction - to the T-lymphocytes. This process is necessary to create effective immune responses and memory and is also relevant in transplant rejection and autoimmune diseases.

In an article published in Journal of Experimental Medicine, the researchers describe a new molecular mechanism that promotes antigen presentation by macrophages to T CD4 lymphocytes. Specifically, they found that the genes that are responsible for expressing antigen-presenting molecules in the macrophages are activated by the protein NFAT5

NFAT5 is known primarily for its role in cells’ adaptation to highly saline environments. Recent studies by the group have revealed new functions of this protein, such as regulating gene expression in immune cells in different contexts. 

The results show that when NFAT5 is eliminated, the communication between macrophages and T cells is interrupted.  

They used skin grafts in mice as a model because antigen presentation is part of the transplant rejection process. On the one hand, in the normal mice rejection occurred when they received a skin transplant from another mouse. But in the cases in which the donors had NFAT5-deficient macrophages, the grafts could survive longer. 

“Consistent with our observations in in vitro trials, our results show that when NFAT5 is eliminated, the communication between macrophages and T cells is interrupted, the latter are not activated and therefore the rejection of skin transplants is attenuated”, say Cristina López-Rodríguez and Jose Aramburu, who coordinate the NFAT5 Proteins and Immune Responses research group. 

This study has also involved scientists from the Biological Research Centre, the National Centre for Cardiovascular Research, the Complutense University of Madrid and the animal facility of the Barcelona Biomedical Research Park and the Barcelona Science Park.

Reference article:

M Buxadé, H Huerga Encabo, M Riera-Borrull, L Quintana-Gallardo, P López-Cotarelo, M Tellechea, S Martínez-Martínez, JM Redondo, J Martín-Caballero, JM Flores, E Bosch, JL Rodríguez-Fernández, J Aramburu and C López-Rodríguez. Macrophage-specific MHCII expression is regulated by a remote Ciita enhancer controlled by NFAT5. Journal of Experimental Medicine, October 2018. DOI: 10.1084/jem.20180314. 

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