الفهرس 
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Abstract
Rare loss of function mutation in interleukin-10 receptor (IL-10R) caused life threatening intestinal inflammation, which is unresponsive to conventional treatment in children younger than 5 years old. Similar to human disease, it was demonstrated that mice lacking IL-10RA exhibit sever early onset colitis at 3-4 weeks old. The colitis is characterized by accumulation of CCR2 dependent immature Ly6C+ macrophages consonant with reduction in mature Ly6C- macrophages. However, whether the changes in the accumulation of recruited macrophages versus the resident mature one is critical for pathology of colitis developed in these mice need to be investigated. Therefore, the current study employed congenic mice strains carrying the susceptibility locus (Cdcs1+/+) and lacking IL10R or both IL10R and CCR2. At the beginning, Cdcs1+/+ mice (C57/B6 background) lacking IL10RA certainly in macrophages were used for investigating the alteration in macrophages subsets associated with intrinsic loss of IL10RA. Our data demonstrated that immature Ly6C+ macrophages increased in frequency within muscularis externa and lamina propria of Cdcs1+/+Il10rafl/flLysMCre+ mice compared to healthy control Cdcs1+/+Il10rafl/flLysMCre-. Lamia propria macrophages like whole colon exhibit increase in percentage of CCR2-expressing cells within immature Ly6C+ both (MHCII- and MHCII+) and mature Ly6C- macrophages associated with decrease in frequency of CD206-expressing cells. Although Muscularis macrophages demonstrated high percentages of CCR2-expressing cells within immature and mature macrophages subsets, small percentages of CD206-expressing cells were preserved in Muscularisexterna of Cdcs1+/+Il10rafl/flLysMCre+ mice.