Innate Immune Response to Encephalomyocarditis Virus Infection Mediated by CD1d

CD1d-reactive natural killer T (NKT) cells can rapidly produce T helper type 1 (Th1) and/or Th2 cytokines, can activate antigen-presenting cell (APC) interleukin-12 (IL-12) production, and are implicated in the regulation of adaptive immune responses. The role of the CD1d system was assessed during infection with encephalomyocarditis virus (EMCV-D), a picornavirus that causes acute diabetes, paralysis and myocarditis. EMCV-D resistance depends on IL-12-mediated interferon-γ (IFN-γ) production. CD1d-deficient mice, which also lack CD1d-reactive NKT cells, were substantially more sensitive to infection with EMCV-D. Infected CD1d knockout mice had decreased IL-12 levels in vitro and in vivo, and indeed were protected by treatment with exogenous IL-12. IFN-γ production in CD1d knockout mice was decreased compared with that in wild-type (WT) mice in response to EMCV-D in vitro, although differences were not detected in vivo. Treatment with anti-asialo-GM1 antibody, to deplete NK cells, caused a marked increase in susceptibility of WT mice to EMCV-D infection, whereas CD1d knockout mice were little affected, suggesting that NK-cell-mediated protection is CD1d-dependent. Therefore, these data indicate that CD1d is essential for optimal responses to acute picornaviral infection. We propose that CD1d-reactive T cells respond to early immune signals and function in the innate immune response to a physiological viral infection by rapidly augmenting APC IL-12 production and activating NK cells

International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis

BackgroundCritical examination of the quality and validity of available allergic rhinitis (AR) literature is necessary to improve understanding and to appropriately translate this knowledge to clinical care of the AR patient. To evaluate the existing AR literature, international multidisciplinary experts with an interest in AR have produced the International Consensus statement on Allergy and Rhinology: Allergic Rhinitis (ICAR:AR).MethodsUsing previously described methodology, specific topics were developed relating to AR. Each topic was assigned a literature review, evidence-based review (EBR), or evidence-based review with recommendations (EBRR) format as dictated by available evidence and purpose within the ICAR:AR document. Following iterative reviews of each topic, the ICAR:AR document was synthesized and reviewed by all authors for consensus.ResultsThe ICAR:AR document addresses over 100 individual topics related to AR, including diagnosis, pathophysiology, epidemiology, disease burden, risk factors for the development of AR, allergy testing modalities, treatment, and other conditions/comorbidities associated with AR.ConclusionThis critical review of the AR literature has identified several strengths; providers can be confident that treatment decisions are supported by rigorous studies. However, there are also substantial gaps in the AR literature. These knowledge gaps should be viewed as opportunities for improvement, as often the things that we teach and the medicine that we practice are not based on the best quality evidence. This document aims to highlight the strengths and weaknesses of the AR literature to identify areas for future AR research and improved understanding

国际过敏与鼻科学共识声明 : 变应性鼻炎

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/1/ICARPrimaryAuthorCOIForms1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/2/ICARSecondaryAuthorCOIForms.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/3/ICARPrimaryAuthorCOIForms2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/4/ICARAuthorCOI2017.8.15.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/5/alr22073_c.pd

国际过敏与鼻科学共识声明 : 变应性鼻炎

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/1/ICARPrimaryAuthorCOIForms1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/2/ICARSecondaryAuthorCOIForms.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/3/ICARPrimaryAuthorCOIForms2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/4/ICARAuthorCOI2017.8.15.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150599/5/alr22073_c.pd