Updated review on immune factors in pathogenesis of Crohn’s disease

Abstract

Although the incidence of Crohn’s disease (CD) in China is not as high as that in European and American countries, there has been a clear increasing trend in recent years. Little is known about its pathogenesis, cause of deferment, and the range of complications associated with the disease. Local and international scholars have presented many hypotheses about CD pathogenesis based on experimental and clinical studies, including genetic susceptibility, immune function defects, intestinal microflora disorders, delayed hypersensitivity, and food antigen stimulation. However, the specific mechanism leading to this immune imbalance, which causes persistent intestinal mucosal damage, and the source of the inflammatory cascade reaction are still unclear. So far, the results of research studies differ locally and internationally. This paper presents the most current research on immune factors in the pathogenesis of CD.

Syngeneic red blood cell–induced extracellular vesicles suppress delayed‐type hypersensitivity to self‐antigens in mice

“…Additionally, DTH reactions to non‐pathogenic antigens underlie the pathogenesis of various immune‐related disorders, including contact dermatitis as well as coeliac and Crohn's diseases . In such conditions, therapeutic strategies to precisely induce immune tolerance to particular antigens, simultaneously preserving immune responsiveness to other antigens, would bring the most beneficial effects.…”

“…Additionally, DTH reactions to non-pathogenic antigens underlie the pathogenesis of various immune-related disorders, including contact dermatitis as well as coeliac and Crohn's diseases. 19,46 In such conditions, therapeutic strategies to precisely induce immune tolerance to particular antigens, simultaneously preserving immune responsiveness to other antigens, would bring the most beneficial effects. In this regard, the currently described mechanism of DTH suppression expands our current understanding of the process of immune regulation via EVs and miRNAs and the possible means of its induction.…”

Spontaneous colitis in IL‐10‐deficient mice was ameliorated via inhibiting glutaminase1

“…However, the exact aetiology is poorly understood, which limits diagnostic and treatment improvements. The interaction between the intestinal barrier and the immune system may play an important role in the pathogenesis of CD …”

“…5 Among the variety of inflammatory cells in the intestine, mucosal CD4 + lymphocytes are believed to play central roles in both the induction and persistence of chronic inflammation by producing pro-inflammatory cytokines. 2,6 Crohn's disease is mainly characterized by an enhanced Th1 response 7,8 together with an increased Th17 immune response, which plays a critical role in the pathogenesis of CD. 9 Local immune balance of intestinal tissue is maintained by regulatory T cells (Tregs) in the intestine that inhibit the proliferation and response of other helper-T cells (Th cells).…”

Integration of immunome with disease-gene network reveals common cellular mechanisms between IMIDs and drug repurposing strategies

“…The pathway enrichment of the DAGs in this DIME-pleiotropy network revealed pathways related to TCR signaling, interleukin signaling, neutrophil degranulation and regulation of TLR ( Supplementary Figure 5A ). As observed in the DIME-pleiotropy network ( Figure 3B ), CD4 + TH1 cells have been implicated in the pathogenesis of both Crohn’s disease and psoriasis 49,50 . Likewise, in the DIME-pleiotropy network ( Figure 3C ) of SSc (MeSH: skin disease) and pulmonary fibrosis (MeSH: respiratory tract disease), we found cell-gene networks between progenitors and pDCs, NK cells, CD4 + TEMRA and CD4 + T regulatory, and other myeloid cells.…”