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This paper reviews the new biologic agents that selectively block the immunologic steps implicated in the pathogenesis of psoriasis. Four strategies have been targeted: reduction of the number of pathogenic T cells; inhibition of T-cell activation and migration; modulation of the immune system; and blockage of the activity of inflammatory cytokines. There are three classes: monoclonal antibodies, fusion proteins and recombinant cytokines or growth factors. The actions, efficacy and side-effect profile of the biologic agents, alefacept, efalizumab, etanercept and infliximab, are reviewed. [ABSTRACT FROM AUTHOR]

The previously observed reduction in peripheral cytotoxic/suppressor T cell populations in subjects with alopecia areata (AA) was confirmed (p <0.001). Moreover, a hitherto undescribed decrease in circulating natural killer cells was noted (p <0.01). These data show that disorders of cellular immunity are present in patients affected with AA and complement the results of other investigations. [ABSTRACT FROM AUTHOR]

There is substantial evidence from experiments of nature that immune competence plays a major part in determining the outcome of anogenital human papillomavirus (HPV) infection. Cellular rather than humoral immunity would appear to be the key to the control and eradication of HPV-induced warts. It seems likely that the HPV early proteins, which are responsible for viral replication (E1 and E2) and for promoting tissue proliferation (E6 and E7) will be the target antigens recognized by antigen-specific T cells. Natural infection is slow to produce an appropriate therapeutic immune response to these proteins, probably because HPV has adopted a strategy to prevent the effective presentation of viral antigens to the host immune system. Human papilomavirus infection is non-lytic so there is little release of viral antigen to professional antigen-presenting cells. Additionally no local pro-inflammatory cytokine production and no local inflammation is induced by HPV infection. An optimal therapeutic strategy for anogenital HPV infection would be, therefore, to accelerate the induction of a strong virus-specific immune response by inducing local inflammation and the cytokines necessary to invoke HPV-specific immunity. [ABSTRACT FROM AUTHOR]