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Indeed, medications previously used to treat autoimmune diseases have later been discovered to exert their action via epigenetic mechanisms. Herein, we review the findings on epigenetics associated with psoriasis, and discuss future perspectives in this field.Systemic lupus erythematosus (SLE) is a life-threatening autoimmune disease that is characterized by dysregulated dendritic cells, T and B cells, and abundant autoantibodies. The pathogenesis of lupus remains unclear. However, increasing evidence has shown that environment factors, genetic susceptibilities, and epigenetic regulation contribute to abnormalities in the immune system. In the past decades, several risk gene loci have been identified, such as MHC and C1q. However, genetics cannot explain the high discordance of lupus incidence in homozygous twins. Environmental factor-induced epigenetic modifications on immune cells may provide some insight. XL177A Epigenetics refers to inheritable changes in a chromosome without altering DNA sequence. The primary mechanisms of epigenetics include DNA methylation, histone modifications, and non-coding RNA regulations. Increasing evidence has shown the importance of dysregulated epigenetic modifications in immune cells in pathogenesis of lupus, and has identified epigenetic changes as potential biomarkers and therapeutic targets. Environmental factors, such as drugs, diet, and pollution, may also be the triggers of epigenetic changes. Therefore, this chapter will summarize the up-to-date progress on epigenetics regulation in lupus, in order to broaden our understanding of lupus and discuss the potential roles of epigenetic regulations for clinical applications.Asthma and rhinitis are complex, heterogeneous diseases characterized by chronic inflammation of the upper and lower airways. While genome-wide association studies (GWAS) have identified a number of susceptible loci and candidate genes associated with the pathogenesis of asthma and allergic rhinitis (AR), the risk-associated alleles account for only a very small percent of the genetic risk. In allergic airway and other complex diseases, it is thought that epigenetic modifications, including DNA methylation, histone modifications, and non-coding microRNAs, caused by complex interactions between the underlying genome and the environment may account for some of this "missing heritability" and may explain the high degree of plasticity in immune responses. In this chapter, we will focus on the current knowledge of classical epigenetic modifications, DNA methylation and histone modifications, and their potential role in asthma and AR. In particular, we will review epigenetic variations associated with maternal airway disease, demographics, environment, and non-specific associations. The role of specific genetic haplotypes in environmentally induced epigenetic changes are also discussed. A major limitation of many of the current studies of asthma epigenetics is that they evaluate epigenetic modifications in both allergic and non-allergic asthma, making it difficult to distinguish those epigenetic modifications that mediate allergic asthma from those that mediate non-allergic asthma. Additionally, most DNA methylation studies in asthma use peripheral or cord blood due to poor accessibility of airway cells or tissue. Unlike DNA sequences, epigenetic alterations are quite cell- and tissue-specific, and epigenetic changes found in airway tissue or cells may be discordant from that of circulating blood. These two confounding factors should be considered when reviewing epigenetic studies in allergic airway disease.Food allergy is a global health problem, particularly in developed countries. It is mainly mediated by Th2 cell and IgE produced by B cells. While the pathogenesis of IgE-mediated food allergy is quite straightforward, the factors that lead to the development of food allergies at any age in children and adults are unclear. Recent studies have revealed that genetics, epigenetics, and environmental exposures contribute to the development of atopy. In this chapter, we discuss the interplay between these three key elements, reveal how epigenetic modifications may mediate genetic susceptibility of food allergies, and explain why epigenetic modifications may be the key in environmental factors mediated-gene expression, leading to the loss of immune tolerance and eventually, the initiation of food allergies. It should be noted that the study of the role of epigenetics in food allergy is still in its infancy, and lags behind research on epigenetics in other fields such as cancer and autoimmune diseases. One of the reasons for this may be the extreme complexity and variability of clinical presentation of food allergy, ranging from less severe forms such as oral allergy syndrome to full-blown anaphylaxis. Research on early exposure has disrupted the previous thinking of avoidance of food allergies to prevent sensitization in children, instead leading to recommendations that early introduction to foods may, in fact, induce tolerance. However, clear and unequivocal guidelines on how to approach this in the clinical setting have not been developed. The coming of the epigenetic era in food allergies is to provide better understanding of pathogenesis of food allergy, as well as providing therapeutic and preventive strategies for this very common condition.Atopic Dermatitis (AD) is a common inflammatory disease with a genetic background. The prevalence of AD has been increasing in many countries. AD patients often have manifestations of pruritus, generalized skin dryness, and eczematous lesions. The pathogenesis of AD is complicated. The impaired skin barrier and immune imbalance play significant roles in the development of AD. Environmental factors such as allergens and pollutants are associated with the increasing prevalence. Many genetic and environmental factors induce a skin barrier deficiency, and this can lead to immune imbalance, which exacerbates the impaired skin barrier to form a vicious cycle (outside-inside-outside view). Genetic studies find many gene mutations and genetic variants, such as filaggrin mutations, which may directly induce the deficiency of the skin barrier and immune system. Epigenetic studies provide a connection between the relationship of an impaired skin barrier and immune and environmental factors, such as tobacco exposure, pollutants, microbes, and diet and nutrients.