We propose that the mechanism by which CD33dim HLA DR+ CD11b- MC contributes to IBD involves the weakening of neutrophil adhesion function due to the absence of CD11b expression, and the induction of high levels of interleukin-1β(IL–1β), IL-6, and tumour necrosis factor-α (TNF-α) by MC (32). Here, IL1B is linked to inflammatory bowel disease.