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Apoptosis is a process of programmed cell death that maintains homeostasis of the skin. Apoptotic cell death regulates keratinocyte proliferation and formation of stratum corneum. The process by which keratinocytes undergo apoptosis is a multistep program mediated by binding of specific death ligands to death receptors or by the release of effector cell granules. Dysfunctional apoptosis has an important role in the development of several skin diseases. Psoriasis is a common chronic inflammatory skin disease characterized by hyperproliferation with incomplete differentiation of epidermal keratinocytes and decreased keratinocyte apoptosis. Psoriatic keratinocytes possess an enhanced ability to resist apoptosis, which might be one of the key pathogenetic mechanisms in psoriasis. In addition, psoriasis is nowadays also recognized as the most prevalent autoimmune disease resulting from aberrant activation of both innate and adaptive immunity. However, the role of cell cytotoxicity mediated by cytotoxic CD8+ T cells and NK cells in psoriasis is as yet unclear. Here, we review the role of different apoptotic pathways in psoriasis.

Infliximab is an anti-tumor necrosis factor-monoclonal antibody shown to be effective in the treatment of moderate-to-severe psoriasis and psoriatic arthritis. We report on the first two patients in Croatia in which the efficacy of infliximab therapy was monitored and evaluated primarily on the basis of cutaneous manifestations of psoriasis. Both patients had severe, treatment-resistant chronic plaque psoriasis and psoriatic arthritis and were on methotrexate therapy before the initiation and throughout the course of infliximab treatment. Infliximab was administered intravenously at a dose of 4 or 5 mg/kg at week 0, 2, 6 and every 8 weeks thereafter. Disease severity was measured before each infusion by means of Psoriasis Area and Severity Index (PASI) score. A remarkable clinical response was achieved in both patients with a 50% or greater improvement in baseline PASI at week 2 after therapy initiation and a 90% or greater improvement at week 6 in one patient and at week 14 in the other. Both patients also reported a significant decline in their arthritis symptoms shortly after the introduction of infliximab. The concomitant use of infliximab and methotrexate in these two patients resulted in rapid and sustained remission of psoriasis with no major adverse effects detected.

This overview highlights the risk of skin diseases arising in workers exposed to ultraviolet radiation (UVR) at their workplace. There is a plethora of skin manifestations in outdoor workers such as seamen, fishermen, farmers after acute intense or long-term exposure to solar UVR, but some cutaneous diseases may also develop in indoor workers exposed to artificial sources. In recent years, investigations of the biological effects and damage caused by UVB and UVA on the skin have improved our understanding of the cellular and molecular mechanisms of photoaging, skin cancer and other skin diseases caused by UVR exposure. The necessity of primary prevention in workers exposed to UVR is emphasized.

In this historical review the authors investigated the treatment of psoriasis through the centuries. There are numerous obstacles in search for the description of psoriasis vulgaris in the works of the great physicians in the antiquity. Most remedies have been developed empirically. During the last two centuries, innumerable drugs have been employed in the treatment of psoriasis. Today dermatologists use the rotational treatment to diminish adverse drug events. In the future psoriasis will probably be cured with the new biological agents.

Psoriasis is a chronic hypeproliferative inflammatory skin disease characterized by abnormal keratinocyte hyperproliferation and differentiation, intra-epidermal accumulation of neutrophil granulocytes, and dermal inflammatory infiltrate that mostly consists of T-cells. Today, psoriasis is definitely recognized as a T-cell-mediated inflammatory disease. Infiltration of T-cells seems to be the primary event that precedes the keratinocyte hyperproliferation. It is suggested that systemic lymphocyte activation is followed by the local accumulation of specific CD4+ T-cells and subsequently by the activation of intradermal CD8+ T-cells. So far, it seems that CD4+ T-cells create an appropriate type-1 cytokine environment for CD8+ T-cells activation that eventually trigger the psoriatic cascade. Thus, T-cells are responsible for initiation and maintenance of psoriasis. The precise mechanism how activated T-cells trigger psoriasis is yet unknown. However, it seems that the specific immune reaction to a putative antigen, mediated by T-cells leads to creation of psoriatic lesions. The immune reaction constantly driven by bacterial superantigens or epidermal self-antigens eventually leads to development of psoriatic lesions. The psoriatic process is a dynamic process that includes interaction between Th1- and Tc1-cells as well as between T-cells and keratinocytes. The better understanding of the immunopathogenesis of psoriasis would allow for development of specific T-cell-targeted and/or cytokine-targeted new therapies.

There is considerable epidemiologic evidence that genetic component plays a key role in the pathogenesis of psoriasis. The disease is multifactorial in origin and shows polygeneic inheritance. In the last decade, there have been significant advances in our understanding of the genetic basis of this common disease. Susceptibility gene characterization and knowledge of the immune basis of psoriasis have better defined the disease pathways involved in the pathogenesis of psoriasis. A number of genetic loci have been identified by genome wide-linkage scans. In particular, the importance of PSORS 1 linkage characterization is emphasized, as this information will help develop more specific diagnostic and prognostic tools.