Chemokines are critical for the inflammatory process in autoimmune diseases such as rheumatoid arthritis (RA). The chemokine receptor-5 (CCR5) mediates chemotaxis by CC-chemokines and is expressed by lymphocytes with the Th1 phenotype and monocyte/macrophages. A 32 bp deletion in the CCR5 (CCR5-⌬32 allele) abolishes receptor expression in homozygotes, while CCR5-⌬32 carriers would express less receptor than wild-type homozygotes. This polymorphism is related to the resistance to HIV-1 infection and progression towards AIDS. We hypothesized that the CCR5-⌬32 allele may modulate the severity of disease in RA. A total of 160 RA-patients (71 and 89 with severe and non-severe phenotypes, respectively) and 500 healthy individuals from the same Caucasian population (Asturias, northern Spain) were genotyped. Carriers of the CCR5-⌬32 allele were at a significantly higher frequency (P = 0.012) in non-severe compared to severe patients (17% vs 4%). Our results suggest that the CCR5-⌬32 polymorphism is a genetic marker related to the severity of RA. Genes and Immunity (2000) 1, 288-289.Keywords: chemokines; CCR5-⌬32 allele; rheumatoid arthritis; disease severity Rheumatoid arthritis (RA) is a systemic chronic inflammatory disease of the joints characterized by the infiltration of the synovial membrane with T lymphocytes and macrophages, and pannus formation over the underlying cartilage and bone. The inflammatory process observed in RA is mediated by chemotactic factors released by the inflamed tissues. Chemokines display a potent chemotactic activity for cells of the immune system, playing an important role in both the destructive and the fibrovasculoproliferative phases of RA.1 The chemokine receptor-5 (CCR5) mediates chemotaxis by the CC-chemokines RANTES, MIP-1␣ and MIP-1␤. This receptor is expressed by lymphocytes exhibiting the Th1-phenotype and by monocytes/macrophages. 2In addition to its role in inflammation, CCR5 also acts as an HIV-1 coreceptor to mediate the first step in cell entry:fusion of the viral envelope with the membrane in the the target CD4 + cell. A 32 bp deletion at the coding region of the CCR5 gene, the CCR5-⌬32 mutation, leads to the expression of reduced amounts of the CCR5 protein in heterozygous individuals.3 CCR5-⌬32 homozygotes do not express the receptor and have nearly complete resistence to HIV-1 infection despite repeated exposure, while heterozygotes progress slowly towards AIDS compared to wild-type homozygotes. 4 The CCR5-

This study analyzed gender-related differences in a cohort of patients with psoriatic spondyloarthropathy (SpA) We performed a retrospective cross-sectional study of 100 patients (mean age 48 +/- 14 years; 63 men, 37 women), diagnosed as having psoriatic SpA on the basis of ESSG criteria. All patients were studied according to a standard protocol, and HLA-B27 and Cw status were analyzed in the study population and their frequencies compared to that of 177 healthy blood donors. The clinical features of PsSpA were compared between men and women by univariate analyses. Twenty-three patients showed isolated axial disease (M:F ratio 3.6:1), 36 had polyaxial disease (M:F ratio 1:1), and 41 showed oligoaxial pattern (M:F ratio 1.7:1). HLA-B27 was correlated with male sex (P=0.002) and isolated axial disease (P=0.016). Univariate analysis showed female sex to be correlated with lower complement levels (P < 0.05), erosive disease (P = 0.05), higher swelling joint count (P = 0.002), and higher scores on the Health Assessment Questionnaire-Specific for SpA (P < 0.05). The HLA-B27 antigen seems to be a defined genetic risk factor only in men with psoriatic SpA. The extent of the spondylitic process is quite similar between the two, although women show poorer functional performance and more aggressive peripheral disease.