Immune protection of helminth-infection and its products in autoimmune diseases
SONG Xiao-rong1,3,XU Yuan-hong2,3,SHEN Ji-long3
1.Department of Cardiac Surgery, Anhui Provincial Hospital Affiliated to Anhui Medical University; Anhui Cardiovascular Research Institute, Hefei 230001, China; 2.Clinical Laboroatory, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China; 3.Department of Microbiology & Parasitology / Province Laboratory of Microbiology&Parasitology/ Anhui Key Laboratory of Zoonoses, Anhui Medical University, Hefei 230032, China
Abstract:The Hygiene Hypothesis suggests that helminth and microbes have been important for shaping and tuning the evolution of the human immune system. The fact that helminth infections were no longer prevalent has led to the emergence of autoimmune inflammatory diseases in developed country. Chronic infections are characterized by a Th2-dominant response as well as an overall down-regulated immune system. This helminth-induced immune-suppression may spill over to unrelated antigens, down-regulate the response to other pathogens. Recent studies have suggested that helminth infection is protective in murine models of autoimmune disorders and asthma. Helminth and its products have showed a prosperous clinical perspective. However, the precise mechanism of the downregulatory immune response remains to be clarified. In this review, we summarize the current progresses of immune regulatory effects of heminth infection and heminth-derived molecules on autoimmune diseases, focusing on the possible molecular mechanism of immune suppression especially.
宋晓蓉,徐元宏,沈继龙. 蠕虫及虫源性分子对自身免疫性疾病的保护作用[J]. 中国人兽共患病学报, 2014, 30(2): 186-190.
SONG Xiao-rong,XU Yuan-hong,SHEN Ji-long. Immune protection of helminth-infection and its products in autoimmune diseases. Chinese Journal of Zoonoses, 2014, 30(2): 186-190.
[1] Elliott DE, Weinstock JV. Helminth-host immunological interactions: prevention and control of immune-mediated diseases[J]. Ann N YAcad Sci, 2012, 1247: 83-96. [2]Allen JE, Maizels RM. Diversity and dialogue in immunity to helminths[J]. Nat Rev Immunol, 2011, 11(6): 375-388. [3]Zheng X, Hu X, Zhou G, et al. Soluble egg antigen from Schistosoma japonicum modulates the progression of chronic progressive experimental autoimmune encephalomyelitis via Th2-shift response[J]. J Neuroimmunol, 2008, 194(1-2): 107-114. [4]Correale J, Farez MF. Parasite infections in multiple sclerosis modulate immune responses through a retinoic acid-dependent pathway[J]. J Immunol, 2013, 191(7): 3827-3837. [5]Walsh KP, Brady MT, Finlay CM, et al. Infection with a helminth parasite attenuates autoimmunity through TGF-beta-mediated suppression of Th17 and Th1 responses[J]. J Immunol, 2009, 183(3): 1577-1586. [6]Gruden-Movsesijan A, Ilic N, Mostarica-Stojkovic M, et al. Mechanisms of modulation of experimental autoimmune encephalomyelitis by chronic Trichinella spiralis infection in Dark Agouti rats[J]. Parasite Immunol, 2010, 32(6): 450-459. [7]Osada Y, Shimizu S, Kumagai T, et al. Schistosoma mansoni infection reduces severity of collagen-induced arthritis via down-regulation of pro-inflammatory mediators[J]. Int J Parasitol, 2009, 39(4): 457-464. [8]Liu Q, Sundar K, Mishra PK, et al. Helminth infection can reduce insulitis and type 1 diabetes through CD25- and IL-10-independent mechanisms[J]. Infect Immun, 2009, 77(12): 5347-5358. [9]El-Ahwany E, Bauiomy IR, Nagy F, et al. T regulatory cell responses to immunization with a soluble egg antigen in Schistosoma mansoni-infected mice[J]. Korean J Parasitol, 2012, 50(1): 29-35. [10]Hubner MP, Stocker JT, Mitre E. Inhibition of type 1 diabetes in filaria-infected non-obese diabetic mice is associated with a T helper type 2 shift and induction of FoxP3+ regulatory T cells[J]. Immunology, 2009, 127(4): 512-522. [11]Ruyssers NE, De Winter BY, De Man JG, et al. Schistosoma mansoni proteins attenuate gastrointestinal motility disturbances during experimental colitis in mice[J]. World J Gastroenterol, 2010, 16(6): 703-712. [12]Smith P, Mangan NE, Walsh CM, et al. Infection with a helminth parasite prevents experimental colitis via a macrophage-mediated mechanism[J]. J Immunol, 2007, 178(7): 4557-4566. [13]Weinstock JV, Elliott DE. Translatability of helminth therapy in inflammatory bowel diseases[J]. Int J Parasitol, 2013, 43(3/4): 245-251. [14]Martin-Orozco N, Chung Y, Chang SH, et al. Th17 cells promote pancreatic inflammation but only induce diabetes efficiently in lymphopenic hosts after conversion into Th1 cells [J]. Eur J Immunol, 2009, 39(1): 216-224. [15]Sun S, Wang X, Wu X, et al. Toll-like receptor activation by helminths or helminth products to alleviate inflammatory bowel disease[J]. Parasit Vectors, 2011, 4: 186-193. [16]Donnelly S, O’Neill SM, Stack CM, et al. Helminth cysteine proteases inhibit TRIF-dependent activation of macrophages via degradation of TLR3[J]. J Biol Chem, 2010, 285(5): 3383-3392. [17]Carvalho L, Sun J, Kane C, et al. Review series on helminths, immune modulation and the hygiene hypothesis: mechanisms underlying helminth modulation of dendritic cell function[J]. Immunology, 2009, 126(1): 28-34. [18]Thomas PG, Carter MR, Da’dara AA, et al. A helminth glycan induces APC maturation via alternative NF-kappa B activation independent of I kappa B alpha degradation[J]. J Immunol, 2005, 75(4): 2082-2090. [19]Breuilh L, Vanhoutte F, Fontaine J, et al. Galectin-3 modulates immune and inflammatory responses during helminthic infection: impact of galectin-3 deficiency on the functions of dendritic cells[J]. Infect Immun, 2007, 75(11): 5148-5157. [20]Melendez AJ, Harnett MM, Pushparaj PN, et al. Inhibition of Fc epsilon RI-mediated mast cell responses by ES-62, a product of parasitic filarial nematodes[J]. Nat Med, 2007, 13(11): 1375-1381. [21]Imai S, Fujita K. Molecules of parasites as immunomodulatory drugs[J]. Curr Top Med Chem, 2004, 4(5): 539-552. [22]Donnelly S, Stack CM, O’Neill SM, et al. Helminth 2-Cys peroxiredoxin drives Th2 responses through a mechanism involving alternatively activated macrophages[J]. FASEB J, 2008, 22(11): 4022-4032. [23]Steinfelder S, Andersen JF, Cannons JL, et al. The major component in schistosome eggs responsible for conditioning dendritic cells for Th2 polarization is a T2 ribonuclease (omega-1)[J]. J Exp Med, 2009, 206(8): 1681-1690. [24]Everts B, Perona-Wright G, Smits HH, et al. Omega-1, a glycoprotein secreted by Schistosoma mansoni eggs, drives Th2 responses[J]. J Exp Med, 2009, 206(8): 1673-1680. [25]Lundy SK, Lukacs NW. Chronic schistosome infection leads to modulation of granuloma formation and systemic immune suppression[J]. Front Immunol, 2013, 4: 39. [26]Khan AR, Fallon PG. Helminth therapies: translating the unknown unknowns to known knowns[J]. Int J Parasitol, 2013, 43: 293-299. [27]Hunter MM, Wang A, Hirota CL, et al. Neutralizing anti-IL-10 antibody blocks the protective effect of tapeworm infection in a murine model of chemically induced colitis[J]. J Immunol, 2005, 174(11): 7368-7375. [28]Melon A, Wang A, Phan V, et al. Infection with Hymenolepis diminuta is more effective than daily corticosteroids in blocking chemically induced colitis in mice[J]. J Biomed Biotechnol, 2010, 2010: 384523.