Boirivant M, Amendola A, Butera A
Department of Infectious, Parasitic and Immune-mediated Diseases, Immune-mediated Disease Section, Istituto Superiore di Sanità, Rome, Italy.
Mucosal Immunol. 2008 Nov;1 Suppl 1:S47-9. doi: 10.1038/mi.2008.52.
Immune homeostasis at mucosal level results from controlled response to intestinal luminal antigens. Recent insights into the nature of inflammatory bowel diseases, derived mainly from studies of experimental models of colonic inflammation, strongly suggest that they can result from a loss of immune tolerance to antigens in the bacterial microflora. Investigations of the regulatory mechanisms operating at the mucosal level suggest that regulatory cells reactive to the intestinal microflora might play a role in cross-reactive protection toward different antigens. Expansion of microflora-reactive regulatory cells by probiotic administration is able to protect from experimental colitis. Characterization of regulatory cells in response to normal commensal flora, the basis of their development and the role of innate immunity in this process might contribute to the understanding of the development of inflammatory bowel diseases.
黏膜水平的免疫稳态源于对肠腔抗原的可控反应。近期对炎症性肠病本质的见解，主要来自对结肠炎症实验模型的研究，强烈表明它们可能是由于对细菌微生物群中抗原的免疫耐受丧失所致。对在黏膜水平起作用的调节机制的研究表明，对肠道微生物群有反应的调节细胞可能在对不同抗原的交叉反应性保护中发挥作用。通过给予益生菌来扩增对微生物群有反应的调节细胞能够预防实验性结肠炎。对响应正常共生菌群的调节细胞进行表征、其发育的基础以及先天免疫在此过程中的作用，可能有助于理解炎症性肠病的发病机制。
