The intestine is an exclusive tissue able to maintain balance between the immune system activation and the tolerance against the very huge amount of harmless antigens that are in contact with the intestinal lumen, including food antigens and mLcroflorD. It is fundamental for our health that our immune system is able to respond with a robust and appropriate response to potential dangerous antigens; but the same reaction against harmless antigens, like commensal bacteria or dietary proteins, could be very dangerous and could give rise to allergies or chronic LnflDmmDtLon that, in the end, can lead to tissue damage or cancer development.

Many immune cells participate in the maintenance of the homeostasis in gut, with the role of understanding how an antigen is a potential danger for the organism and being silenced in response to commensal bacteria and food antigens. НLs complex landscape includes T and B lymphocytes, natural killer cells, innate lymphoid cells, eosinophil and mononuclear phagocytes: dendritic cells and macrophages. Among the latter, monocyte-derived macrophages, expressing the CX3CR1 receptor, constitute the most abundant population and focused on the role of CX3CR1+ macrophages in both steady state and acute colitis.

 In the last few years intensive research has been performed in order to clarify the role of these immune cells in the maintenance of homeostasis, but still, contrasting results have been reported regarding their role in the control of LnflDmmDtor\ response in the intestine. Considering this confused landscape, our paper aimed to clarify the role of CX3CR1+ cells in the development of acute colitis. By using mice lacking the receptor (CX3CR1GFP/GFP mice) we demonstrated that the absence of CX3CR1 on gut macrophages leads to a more severe degree of DSS-induced colitis, higher colon LnfiltrDtLon of LnflDmmDtor\ macrophages and Н lymphocytes and higher expression of LnflDmmDtor\ cytokines. Macrophages in the intestinal mucosa are considered mononuclear phagocytes that originate from a common myeloid progenitor which can also into dendritic cells

Regards
Sarah Eve
Journal of Mucosal Immunology Research