Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection

Takei, Izumi; Asaba, Yoshiaki; Kasatani, Tomohiro; Maruyama, Taro; Watanabe, Kenji; Yanagawa, Tatsuo; Saruta, Takao; Ishii, Toshiharu

doi:10.1016/0896-8411(92)90184-r

Cited by 78 publications

(44 citation statements)

References 26 publications

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“…Indeed, past studies revealed that NOD mice in gnotobiotic surroundings have a higher incidence of diabetes [37][38][39][40][41]. These observations, along with our current results and previous data from others, suggest that environmental stimuli, be they via active infections [20][21][22][23][24][25], immunizations [16][17][18][19], soluble antigens, or even dietary factors [42,43], allow for activation of T cells that exert a regulatory effect on the pathogenic potential of self-reactive lymphocytes. On a related note, studies among human patients have also suggested that infections early in life prevent the onset of autoimmune diabetes [44].…”

Section: Discussionsupporting

confidence: 74%

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Regulation of autoimmune diabetes by non‐islet‐specific T cells — a role for the glucocorticoid‐induced TNF receptor

et al. 2004

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Diabetogenic BDC2.5 CD4 T cells induce diabetes when injected into NOD.scid mice. However, when co‐transferred with the OVA‐specific DO11.10 CD4 T cells, BDC2.5 T cells failed to cause diabetes. This inhibition depended upon the stimulation of DO11.10 T cells only with soluble OVA, which skewed their differentiation to a Th2‐type pattern of cytokine secretion in vivo. However, in vivo neutralization of IL‐4, IL‐10 or TGF‐β using monoclonal antibodies did not prevent the inhibition whereas treatment with an antibody against the glucocorticoid‐induced TNF receptor abrogated the protection from disease. In the protected mice, the diabetogenic T cells could be isolated from their spleens and shown to transfer diabetes when injected into new NOD.scid recipients. Thus, the inhibition took place without the physical or functional elimination of the diabetogenic T cells.

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Section: Discussionsupporting

confidence: 74%

“…For example in NOD mice and BB rats, stimulation with bacteria such as BCG or mycobacteria incorporated in complete Freund's adjuvant (CFA) resulted in marked suppression of diabetes [16][17][18][19]. Moreover, in the NOD model, viral infections or helminth infections also protected from diabetes [20][21][22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Regulation of autoimmune diabetes by non‐islet‐specific T cells — a role for the glucocorticoid‐induced TNF receptor

et al. 2004

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“…As discussed above, epidemiological studies provide evidence that infectious events occurring during early childhood might have the ability to prevent or delay type 1 diabetes development (75). The ability of viral infections to abrogate autoimmune diabetes was also reported in different animal models using not only CVB3 (35), but also LCMV (46,76,77), EMC-DV (38), mouse hepatitis virus (78), and lactate dehydrogenase virus (79). Interestingly, both acute and persistent viral infections appear capable of modulating the immune system in a diabetes-preventive fashion.…”

Section: Insight From Experimental Workmentioning

confidence: 97%

Viral Trigger for Type 1 Diabetes

2008

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“…Monkey rotavirus RRV (at birth) [70,71] Monkey rotavirus RRV (12 weeks) [72] Lymphocytic choriomeningitis virus [73,74] Lactate dehydrogenase virus [75] Mouse hepatitis virus [76] Murine gammaherpes virus-68 [77] Coxsackie B3 & B4 viruses [73,78,79] Coxsackie B4 virus (at 8 weeks) [80] Salmonella typhimurium [58] Mycobacterium avium [81] Microbial antigens & products…”

Section: Microbial Infectionsmentioning

confidence: 99%

Helminth Infection and Type 1 Diabetes

Zaccone¹,

Hall²

2012

Rev Diabet Stud

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■ AbstractThe increasing incidence of type 1 diabetes (T1D) and autoimmune diseases in industrialized countries cannot be exclusively explained by genetic factors. Human epidemiological studies and animal experimental data provide accumulating evidence for the role of environmental factors, such as infections, in the regulation of allergy and autoimmune diseases. The hygiene hypothesis has formally provided a rationale for these observations, suggesting that our coevolution with pathogens has contributed to the shaping of the present-day human immune system. Therefore, improved sanitation, together with infection control, has removed immunoregulatory mechanisms on which our immune system may depend. Helminths are multicellular organisms that have developed a wide range of strategies to manipulate the host immune system to survive and complete their reproductive cycles successfully. Immunity to helminths involves profound changes in both the innate and adaptive immune compartments, which can have a protective effect in inflammation and autoimmunity. Recently, helminth-derived antigens and molecules have been tested in vitro and in vivo to explore possible applications in the treatment of inflammatory and autoimmune diseases, including T1D. This exciting approach presents numerous challenges that will need to be addressed before it can reach safe clinical application. This review outlines basic insight into the ability of helminths to modulate the onset and progression of T1D, and frames some of the challenges that helminth-derived therapies may face in the context of clinical translation.

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Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection

Cited by 78 publications

References 26 publications

Regulation of autoimmune diabetes by non‐islet‐specific T cells — a role for the glucocorticoid‐induced TNF receptor

Regulation of autoimmune diabetes by non‐islet‐specific T cells — a role for the glucocorticoid‐induced TNF receptor

Viral Trigger for Type 1 Diabetes

Helminth Infection and Type 1 Diabetes

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