**1. Introduction**

Wound healing in the intestine is a critical process affecting the prognosis of inflammatory bowel disease (IBD) [1]. Failure of healing could result in prolonged hospitalization, critical illness, and even death. Intestinal wound healing is consisted of three cellular events: restitution, proliferation, and differentiation of epithelial cells adjacent to the wounded area [2]. After intestinal tissue damage, the initial response is dominated by a proinflammatory type 1 immune response, whereas during the wound repair process, a more anti-inflammatory type 2 immune response will dominate to promote tissue regeneration and maintain tissue homeostasis [3]. A diverse array of evolutionarily ancient hematopoietic immune cell types, including lymphocytes, dendritic cells (DCs), monocytes, macrophages, and granulocytes, participate in this process. These immune cells secrete large amounts of cytokines and growth factors to signal to local tissue progenitors and stromal cells and promote wound repair. Here, we will discuss the contribution of four major immune cell types (neutrophils, macrophages, and regulatory T cells (Treg) and innate lymphoid cells (ILCs)) and four cytokines (interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), IL-6, and IL-22) to the wound healing process in the intestine (Figure 1).

**Figure 1.** Immune cells and cytokines are contributing to intestinal wound repair. Four major immune cell types (neutrophils, macrophages, Treg) and ILCs), four cytokines (IL-10, TNF-<sup>α</sup>, IL-6, and IL-22) and their corresponding receptors are involved in stem cell renew and wound healing process in the intestine.
