Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are autoantibody-mediated diseases clinically characterized by blistersanderosions of skin and/or mucous membranes. Immune imbalance and antibody generation are the key pathologies of autoimmune bullous diseases. Recently, a large number of studies have shown that T cell subsets, which are critical players in autoimmunity, exhibit a range of abnormalities and drive immunopathogenesis and skin inflammation in PV and BP. T helper (Th)1 cells mediate pro-inflammatory or immune responses through IFN-γ and Th2-derived cytokines, such as IL-4, can promote B cell proliferation, antibody production and immunoglobulin class-switching. Th17 cells promote inflammatory response and skin damage, while regulatory T cells suppress autoreactive CD4+ T cell activation and help control inflammation. T follicular helper cells cross-talk with B cells and facilitate autoantibody production. In this review, we discuss the immune features of PV and BP, with a focus on the aberrations in T cell subsets, such as Th1 cells, Th2 cells, Th17 cells, regulatory T cells, T follicular helper cells, CD8+ T cells, γδ T cells and resident memory T cells in the pathogenesis of PV and BP. Improved understanding of biological and immunological functions of T cell subsets in patients with autoimmune skin disorders will offer unique opportunities for the recognition of treatment targets for these complex diseases.As part of a landmark review of the antigen excess, Jacobs et al. (Autoimmunity Reviews 2015;14160-167) contrast how immunoassay “interference” by non-target biomolecules can cause spurious readings for clinical diagnostic tests. The purpose of the present Letter is to complement and analytically extend this description by Jacobs et al. by briefly presenting a generalized mathematical model of immunoassay interference that is derived from a simple mechanistic system of differential equations. Derivation includes expressions for the location of the peak concentration of bound reporter as well as that maximum concentration of target biomolecule at which immunoassay interference drives concentration of bound reporter to zero. This parsimonious, mechanistic, and generalized model may prove foundational to analytic study of immunoassay interference. More comprehensive models for specific classes of immunoassays have and can be developed.Primary forms of minimal change disease and focal segmental glomerulosclerosis are rare podocytopathies and clinically characterized by nephrotic syndrome. Glucocorticoids are the cornerstone of the initial immunosuppressive treatment in these two entities. Especially among adults with minimal change disease or focal segmental glomerulosclerosis, relapses, steroid dependence or resistance are common and necessitate re-initiation of steroids and other immunosuppressants. Effective steroid-sparing therapies and introduction of less toxic immunosuppressive agents are urgently needed to reduce undesirable side effects, in particular for patients whose disease course is complex. Rituximab, a B cell depleting monoclonal antibody, is increasingly used off-label in these circumstances, despite a low level of evidence for adult patients. Hence, critical questions concerning drug-safety, long-term efficacy and the optimal regimen for rituximab-treatment remain unanswered. Evidence in the form of large, multicenter studies and randomized controlled trials are urgently needed to overcome these limitations.Epidemiological studies have identified vitamin D (25(OH)D) deficiency to be highly prevalent among patients with inflammatory bowel disease (IBD), and low serum levels correlate with a higher disease activity and a more complicated disease course. The link to IBD pathogenesis has been subject of investigations, primarily due to the distinct immunological functions of vitamin D signaling, including anti-inflammatory and anti-fibrotic actions. Vitamin D is a pleiotropic hormone that executes its actions on cells through the vitamin D receptor (VDR). A leaky gut, i.e. an insufficient intestinal epithelial barrier, is thought to be central for the pathogenesis of IBD, and emerging data support the concept that vitamin D/VDR signaling in intestinal epithelial cells (IECs) has an important role in controlling barrier integrity. DCZ0415 Here we review the latest evidence on how vitamin D promotes the interplay between IECs, the gut microbiome, and immune cells and thereby regulate the intestinal immune response. On the cellular level, vitamin D signaling regulates tight junctional complexes, apoptosis, and autophagy, leading to increased epithelial barrier integrity, and promotes expression of antimicrobial peptides as part of its immunomodulating functions. Further, intestinal VDR expression is inversely correlated with the severity of inflammation in patients with IBD, which might compromise the positive effects of vitamin D signaling in patients with flaring disease. Efforts to reveal the role of vitamin D in the pathophysiology of IBD will pave the road for the invention of more rational treatment strategies of this debilitating disease in the future.Polymyalgia rheumatica (PMR) is a frequent rheumatic condition among people over 50 years of age. Despite its frequent association with giant cell arteritis (GCA), PMR can be isolated. Its pathophysiology is poorly understood. Nevertheless, many studies are ongoing; 98 studies are currently referenced in ClinicalTrials.org involving several conventional and targeted therapies. In this review, we synthetize the current knowledge about PMR pathophysiology according to genetic and immunogenetic, immunologic, antibody and aging data. Immunogenetic data are mainly related to the HLA system and the association between the HLA-DRB1 and PMR. Few studies are also about immunogenetics of proinflammatory interleukins (i.e. IL-6). The decrease of CD8+Tcells and the strong increase of IL-6 where the main elements of PMR’s pathophysiology until the recent years. The disturbance of B cell homeostasis, the search for IL-6 secretion by the innate immune system, the role of aging, are new elements revealed by recent studies. Aging might be a key element to consider as PMR occurs in patients over 50 years of age.