Mouse IL-1α(Interleukin 1 Alpha) ELISA Kit

Objective: This study determined whether interleukin 1 (IL1) polymorphisms are associated with susceptibility to systemic lupus erythematosus (SLE). Methods: A meta-analysis was conducted on the associations between the IL1A, IL1B, and IL1 receptor antagonist (IL1 RN) polymorphisms and SLE. Results: A total of 15 studies involving 1956 SLE cases and 2347 controls were included in the meta-analysis. The meta-analysis showed an association between SLE and the IL1A -889 T allele in the overall population and Europeans (OR = 0.858, 95% CI = 0.737-0.986, p = 0.032; OR = 0.827, 95% CI = 0.687-0.994, p = 0.043). Meta-analysis of the IL1 RN polymorphism revealed an association with SLE in all study subjects (OR for IL1RN*2 = 1.539, 95% CI = 1.266-1.871, p = 1.5 x 10(-2)) and in Europeans and Asians (OR = 1.483, 95% CI = 1.187-1.852, p = 0.001; OR = 1.787, 95% CI = 1.167-2.736, p = 0.008). No associations were found between SLE and the IL1B -511 C/T, 3953 C/T, and IL1A +4845 G/T polymorphisms. Conclusions: This meta-analysis suggests IL1A 889 C/T polymorphism is associated with susceptibility to SLE in Europeans, and that the IL1 RN*2 allele is associated with susceptibility to SLE in Europeans and Asians. (C) 2013 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

Reactive microglia and infiltrating peripheral monocytes have been implicated in many neurodegenerative diseases of the retina and CNS. However, their specific contribution in retinal degeneration remains unclear. We recently showed that peripheral monocytes that infiltrate the retina after ocular injury in mice become permanently engrafted into the tissue, establishing a proinflammatory phenotype that promotes neurodegeneration. In this study, we show that microglia regulate the process of neuroglia remodeling during ocular injury, and their depletion results in marked upregulation of inflammatory markers, such as Il17f, Tnfsf11, Ccl4, Il1a, Ccr2, Il4, Il5, and Csf2 in the retina, and abnormal engraftment of peripheral CCR2(+) CX3CR1(+) monocytes into the retina, which is associated with increased retinal ganglion cell loss, retinal nerve fiber layer thinning, and pigmentation onto the retinal surface. Furthermore, we show that other types of ocular injuries, such as penetrating corneal trauma and ocular hypertension also cause similar changes. However, optic nerve crush injury-mediated retinal ganglion cell loss evokes neither peripheral monocyte response in the retina nor pigmentation, although peripheral CX3CR1(+) and CCR2+ monocytes infiltrate the optic nerve injury site and remain present for months. Our study suggests that microglia are key regulators of peripheral monocyte infiltration and retinal pigment epithelium migration, and their depletion results in abnormal neuroglia remodeling that exacerbates neuroretinal tissue damage. This mechanism of retinal damage through neuroglia remodeling may be clinically important for the treatment of patients with ocular injuries, including surgical traumas.