Psoriatic Arthritis: A Guide for Dermatology Nurses

Alice B. Gottlieb, MD, PhD

Disclosures

Dermatology Nursing. 2003;15(2) 

In This Article

Role of TNF in Pathogenesis and TNF Inhibitors in Treating PsA

Cytokines are molecular messengers that interact with cell receptors and are involved in regulating inflammatory and immunologic responses to injury. TNF is a cytokine that plays a central role in the pro- inflammatory disease process of PsA. TNF is produced by multiple cells including macrophages, keratinocytes, lymphocytes, and antigen-presenting cells (Bonifati & Ameglio, 1999). High concentrations of TNF are found in skin, blister fluid, sera, synovial fluid, and synovium of patients with PsA (Bonifati et al., 1994; Ettehadi, Greaves, Wallach, Aderka, & Camp, 1994; Partsch et al., 1997; Ritchlin et al., 1998). The increased concentrations of TNF correlate with disease severity and psoriasis area and severity index (PASI) scores (Gottlieb et al., 2002; Mease, 2001; Mussi et al., 1997). Excess TNF can trigger a cascade of events that lead to inflammation, cartilage damage, and excessive keratinocyte proliferation and abnormal differentiation. The resulting consequences and actions of TNF in PsA are profiled in Table 2 (Gottlieb et al., 2002; Zabraniecki & Fournié, 2001).

TNF inhibition is a promising approach to the treatment of PsA. TNF inhibitors are biologic molecules produced through recombinant DNA techniques. They block the actions of TNF by binding to circulating and membrane-bound TNF, thus inactivating its destructive effects (Iyer, Yamauchi, & Lowe, 2002; Mease, 2001).

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