Psoriasis is a chronic skin disorder of unsolved pathogenesis affecting skin in 2-3% of the general population. Research into the pathogenesis of psoriasis has profited from suitable animal models. Previously, we reported on the CD18 hypomorphic (CD18(hypo)) PL/J mouse model clinically resembling human psoriasis, which is characterized by reduced expression of the common chain of beta(2)-integrins (CD11/CD18) to only 2-16% of wild-type levels. Aside from common clinical and pathophysiological features shared with human psoriasis, the psoriasiform skin disease in CD18(hypo) PL/J mice also depends on the presence of CD4(+) T-cells. This review focuses on the role of activated macrophages in the pathogenesis of CD18(hypo) T-cell-mediated mouse model of psoriasis, and extends our understanding in unrestrained pathogenic T-cells whose activation may be crucial for the recruitment and activation of macrophages within skin. The findings in the CD18(hypo) PL/J model are discussed in the context of current literatures of human and other autoimmune disorders.