Tumor necrosis factor-α inhibitor-associated adverse cutaneous reactions are common in patients with inflammatory bowel disease. Infection-related dermatoses and psoriasiform eruptions are seen most frequently. We describe a follicular psoriasiform eruption that appeared during treatment with infliximab in two adolescents with Crohn's disease.

Depending on ethnicity and on social conditions, between 40 and 90 % of the population is infected with human cytomegalovirus (HCMV). In immunocompetent patients, the virus may cause an acute disease and then revert to a state of latency, which enables its coexistence with the human host. However, in cases of immunosuppression or in neonatal infections, HCMV can cause serious long-lasting illnesses. HCMV has developed multiple mechanisms in order to escape its elimination by the immune system, specifically by two killer cell types of the adaptive and the innate immune systems; cytotoxic T lymphocytes (CTL) and natural killer (NK) cells, respectively. Another fascinating aspect of HCMV is that like other highly developed herpesviruses, it expresses its own unique set of microRNAs. Here, we initially describe how the activity of NK cells is regulated under normal conditions and during infection. Then, we discuss what is currently known about HCMV microRNA-mediated interactions, with special emphasis on immune modulation and NK cell evasion. We further illustrate the significant modulation of cellular microRNAs during HCMV infection. Although, the full target spectrum of HCMV microRNAs is far from being completely elucidated, it can already be concluded that HCMV uses its "multitasking" microRNAs to globally affect its own life cycle, as well as important cellular and immune-related pathways.

Human cytomegalovirus (HCMV) is a highly clinically relevant pathogen. It efficiently infects large proportion of the adult population around the world, and it establishes lifelong latency. In healthy adults, the virus usually does not cause serious or long-lasting injuries; however, in immunocompromised or immune-suppressed patients (like transplant recipients), infection with HCMV can cause serious illnesses and affect many organs. This is also true in cases of congenital infections. In order to introduce novel antiviral interventions and perhaps even therapeutic agents, a better understanding of the viral life cycle, its tropism, and the ways by which it escapes immune elimination is mandatory. In this special issue of Seminars in Immunopathology, we attempt to establish a multifaceted integrative view of the virus and discuss future implications of our current knowledge.The effort to introduce effective treatment for congenital HCMV infections is a clinical and scientific challenge, and may advance through novel fetal-maternal interface models HCMV infections are especially dangerous during pregnancy. Congenital infections can cause intrauterine growth restriction or severe injuries in various body systems in newborns. This makes these infections a highly relevant clinical entity that awaits the introduction of novel and efficient methods of therapy. In the review by Weisblum et al., we are introduced to the various aspects of congenital HCMV infections, with special emphasis on the need for "true-to-life" models of the maternal-fetal interface. The long road to successful novel therapies and vaccines begins in the establishment of experimental models that highly resemble the conditions of the human body. However, the species-specificity of HCMV presents an inherent difficulty in the establishment of good animal model. For that reason, much of our knowledge of maternal-fetal interface events during HCMV infection comes from histological analysis of in vivo infected placental tissues and from various in vitro cultures of human cells. These as well as guinea pig and mouse models have contributed to our knowledge, but lack the ability to fully demonstrate the true pathogenesis and kinetics of congenital HCMV infection in humans. A recently established "organ-culture" model, in which human decidual tissues are maintained as a multicelltype organ, allows us to reveal more aspects of the congenital infection, such as cellular tropism and kinetics. It can also serve as a "living" test ground for novel antiviral treatments and interventions. HCMV-encoded viral Fcγ receptors protect infected cells from immune cellsKnowing the possible serious consequences of HCMV infections, like in the case of congenital infection or infections of immunocompromised patients, we will now zoom in to examine the virus and its pathogenic and stealth promoting elements in the molecular scale. CMV uses significant portions of its vast genome to resist and counteract host immune activation. In a review of CMV-encoded viral Fcγ receptors (v...

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