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首页> 外文期刊>Current Medicinal Chemistry >Advances in the Treatment of Autoimmune Diseases; Cellular Activity, Type-1/Type-2 Cytokine Secretion Patterns and their Modulation by Therapeutic Peptides
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Advances in the Treatment of Autoimmune Diseases; Cellular Activity, Type-1/Type-2 Cytokine Secretion Patterns and their Modulation by Therapeutic Peptides

机译:自身免疫性疾病的治疗进展;细胞活性,1型/ 2型细胞因子分泌模式及其对治疗性肽的调节

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Autoimmune diseases are many, have an overall prevalence of about 3% of the world population, affecting more women than men, and their incidence is influenced by genetics and the environment. It is currently thought that the immune response of a genetically predisposed individual to an environmental pathogen, under the influence of inadequate or non-functional immunoregulatory mechanisms, can lead to the development of an autoimmune disease. Advances in the treatment of autoimmune diseases follow a better understanding of the abnormalities in the cellular activity pathways and the resulting, often permanent, imbalance of the pro- and anti-inflammatory cytokine expression profiles. Over the past few years, there has been a dramatic change in the therapeutic regimens employed in autoimmune diseases, with soluble receptors, monoclonal antibodies and molecular mimetics enhancing or gradually replacing conventional immunosuppressive therapies. New biologicals have been developed, targeting defined pathways of the adaptive immune response. One approach towards the therapeutic management of autoimmune diseases involves the design and use of peptide analogs of disease-associated epitopes to be used as immunomodulatory drugs. Peptides can target cell-functions directly, by interfering with the formation of the tri-molecular complex MHCPeptide- TCR, and/or they can target soluble mediators such as cytokines or their receptors, eventually replacing monoclonal antibody therapies. This review offers an update on the treatment modalities of certain prototypic autoimmune diseases, based on the current knowledge of disease pathogenesis, with emphasis on cell activation and cytokine expression profiles.
机译:自身免疫性疾病很多,总患病率约占世界人口的3%,妇女受累的人数多于男子,其发病率受到遗传和环境的影响。当前认为,遗传上易患病的个体对环境病原体的免疫应答在免疫调节机制不足或功能失调的影响下可导致自身免疫疾病的发展。对自身免疫性疾病的治疗进展是对细胞活性途径的异常以及由此导致的(通常是永久性的)促炎性和抗炎性细胞因子表达谱失衡的更好理解。在过去的几年中,自身免疫性疾病的治疗方案发生了巨大变化,可溶性受体,单克隆抗体和分子模拟物增强或逐渐取代了传统的免疫抑制疗法。已经开发了针对适应性免疫应答的确定途径的新的生物制剂。自身免疫性疾病的治疗管理的一种方法涉及设计和使用与疾病相关的表位的肽类似物作为免疫调节药物。肽可通过干扰三分子复合物MHCPeptide-TCR的形成直接靶向细胞功能,和/或它们可靶向可溶性介体,例如细胞因子或其受体,最终取代单克隆抗体疗法。这篇综述基于疾病发病机理的最新知识,提供了某些原型自身免疫性疾病治疗方式的更新,重点是细胞激活和细胞因子表达谱。

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