Explore the vast range of titles available.

Celiac disease (CD) is an autoimmune condition affecting the small intestine, triggered by the ingestion of gluten, the protein fraction of wheat, barley, and rye. There is a strong linkage between CD and HLA-DQ2 and HLA-DQ8 haplotypes. Multiple case reports and small series suggest concordance between CD and other autoimmune disorders. This paper provides a brief overview of the pathogenesis of CD and reviews the literature regarding associations between CD and other autoimmune diseases, including the potential effects of gluten-free diet therapy on the prevention or amelioration of associated diseases.

Developed societies, although having successfully reduced the burden of infectious disease, constitute an environment where metabolic, cardiovascular, and autoimmune diseases thrive. Living in westernized countries has not fundamentally changed the genetic basis on which these diseases emerge, but has strong impact on lifestyle and pathogen exposure. In particular, nutritional patterns collectively termed the “Western diet”, including high-fat and cholesterol, high-protein, high-sugar, and excess salt intake, as well as frequent consumption of processed and ‘fast foods’, promote obesity, metabolic syndrome, and cardiovascular disease. These factors have also gained high interest as possible promoters of autoimmune diseases. Underlying metabolic and immunologic mechanisms are currently being intensively explored. This review discusses the current knowledge relative to the association of “Western diet” with autoimmunity, and highlights the role of T cells as central players linking dietary influences to autoimmune pathology.

Purpose of ReviewThe goal of this review is to summarize the field to date and to discuss strengths and limitations of low-level laser (light) therapy (LLLT) for the future investigation as a treatment of inflammatory disease.Recent FindingsLLLT is a promising therapeutic, particularly for those diseases of skin and joints because they are most accessible to treatment. Indeed, the known mechanisms of LLLT support its use for anti-inflammatory purposes, as well as stimulation of tissue growth and repair. Although the standard of care for the majority of inflammatory diseases is immunosuppressive agents such as corticosteroids with undesirable toxicities, LLLT offers a unique approach by being non-invasive and incurring minimal side effects. It is also relatively inexpensive and accessible and even has the possibility to be patient directed at home.SummaryThere is evidence that LLLT is able to modulate the immune system at the skin and joint, and it has been shown to be efficacious in humans by affecting bacterial colonization as it may pertain to chronic rhinosinusitis. However, there is variability in the methods of laser application as well as a lack of evidence for laser type, dose-ranging studies, and wavelength selection that create barriers to the implementation of LLLT without further more rigorous and standardized study. The heterogeneity makes it difficult to draw strong conclusions about the efficacy of LLLT and its mechanisms.

Ankylosing spondylitis is an insidiously progressive and debilitating form of arthritis involving the axial skeleton. The long delay in diagnosis and insufficient response to currently available therapeutics both advocate for a greater understanding of disease pathogenesis. Genome-wide association studies of this highly genetic disease have implicated specific immune pathways, including the interleukin (IL)-17/IL-23 pathway, control of nuclear factor kappa B (NF-κB) activation, amino acid trimming for major histocompatibility complex (MHC) antigen presentation, and other genes controlling CD8 and CD4 T cell subsets. The relevance of these pathways has borne out in animal and human subject studies, in particular, the response to novel therapeutic agents. Genetics and the findings of autoantibodies in ankylosing spondylitis revisit the question of autoimmune vs. autoinflammatory etiology. As environmental partners to genetics, recent attention has focused on the roles of microbiota and biomechanical stress in initiating and perpetuating inflammation. Herein, we review these current developments in the investigation of ankylosing spondylitis pathogenesis.

Purpose of ReviewTo provide clinicians with an understanding of risk factors associated with fatal anaphylaxis, and to promote individualized management plans with patients based upon key aspects of their clinical history.Recent FindingsWhile anaphylaxis can affect a significant percentage of the general population, death from anaphylaxis remains a rare outcome. The presence of asthma and peanut or tree nut allergy is associated with higher risk for severe or fatal anaphylaxis from foods. Specific triggers (medications, venom), underlying comorbid conditions, age, and use of some medications can also impact risk and warrant different counseling and management strategies.SummaryAnaphylaxis is a rapidly progressive systemic reaction with multiple different causes and encompasses a wide degree of severity in clinical presentation and risk for future episodes. Individualized management, discussion of risk, and shared decision making should occur with each patient and in consideration of their personal risk factors.

Purpose of ReviewThe purpose of this review is to provide a framework to distinguish Blau syndrome/Early Onset Sarcoidosis and Sarcoidosis clinically. We also discuss relevant differences in genetics, pathogenesis, and management of these diseases.Recent FindingsBlau syndrome and Sarcoidosis share the characteristic histologic finding of noncaseating granulomas as well as some similar clinical characteristics; nevertheless, they are distinct entities with important differences between them. Blau syndrome and Early Onset Sarcoidosis are due to one of numerous possible gain-of-function mutations in NOD2, commonly presenting before age 5 with a triad of skin rash, arthritis, and uveitis. However, as more cases are reported, expanded clinical manifestations have been described. In systemic Sarcoidosis, there are numerous susceptibility genes that have been identified, and disease is thought to result from an environmental exposure in a genetically susceptible host. It most often presents with constitutional symptoms and pulmonary involvement and typically affects adolescents and adults.SummaryThis paper reviews the similarities and differences between Blau syndrome and Sarcoidosis. We also discuss the importance of distinguishing between them, particularly with regard to prognosis and outcomes.

Purpose of ReviewInadequate health literacy is common among American adults, but little is known about the impact of health literacy in rheumatic diseases. The purpose of this article is to review studies investigating health literacy and its association with clinical outcomes in systemic lupus erythematosus (SLE).Recent FindingsSeveral validated health literacy measures have been examined in SLE patients. Low health literacy is associated with worse patient-reported outcomes and lower numeracy with higher disease activity. Two studies found no association of low health literacy with medication adherence. One randomized controlled trial tested a medication decision aid among patients with low health literacy.SummaryWe found a paucity of studies exploring health literacy in SLE. Low health literacy is associated with worse patient-reported outcomes and limited numeracy with higher disease activity in SLE. Further studies are needed exploring the impact of low health literacy on clinical outcomes and the effectiveness of literacy-sensitive interventions.

Purpose of ReviewThe purpose of this review is to recognize clinical features of Paget’s disease of bone and to describe how the osteoclast, a myeloid-derived cell responsible for bone resorption, contributes to the disease.Recent FindingsRecent studies have identified several variants in SQSTM1, OPTN, and other genes that may predispose individuals to Paget’s disease of bone; studies of these genes and their protein products have elucidated new roles for these proteins in bone physiology.SummaryUnderstanding the pathologic mechanisms in the Pagetic osteoclast may lead to the identification of future treatment targets for other inflammatory and autoimmune diseases characterized by abnormal bone erosion and/or osteoclast activation.

Purpose of ReviewThe review provides an update on the diagnosis, pathogenesis, and treatment of cutaneous lupus erythematosus (CLE).Recent FindingsDiagnostic challenges exist in better defining CLE as an independent disease distinct from systemic lupus erythematosus with cutaneous features and further classifying CLE based on clinical, histological, and laboratory features. Recent mechanistic studies revealed more genetic variations, environmental triggers, and immunologic dysfunctions that are associated with CLE. Drug induction specifically has emerged as one of the most important triggers for CLE. Treatment options include topical agents and systemic therapies, including newer biologics such as belimumab, rituximab, ustekinumab, anifrolumab, and BIIB059 that have shown good clinical efficacy in trials.SummaryCLE is a group of complex and heterogenous diseases. Future studies are warranted to better define CLE within the spectrum of lupus erythematosus. Better insight into the pathogenesis of CLE could facilitate the design of more targeted therapies.

The possible role of infections in driving autoimmune disease (AD) has long been debated. Many theories have emerged including release of hidden antigens, epitope spread, anti-idiotypes, molecular mimicry, the adjuvant effect, antigenic complementarity, or simply that AD could be a direct consequence of activation or subversion of the immune response by microbes. A number of issues are not adequately addressed by current theories, including why animal models of AD require adjuvants containing microbial peptides in addition to self tissue to induce disease, and why ADs occur more often in one sex than the other. Reviews published in the past 3 years have focused on the role of the innate immune response in driving AD and the possible role of persistent infections in altering immune responses. Overall, recent evidence suggests that microbes activating specific innate immune responses are critical, while antigenic cross-reactivity may perpetuate immune responses leading to chronic autoinflammatory disease.