The author has provided evidence that intrarenal crosstalk between DCs and T cells causes mutual activation of these cell types. The resulting proinflammatory reaction further recruits immune effector cells that drive progression of renal disease. This mechanism may be of general relevance in immunology and also applies to diseases affecting other organs. For example, a subsequent study demonstrated a similar mechanism in herpes virus infection of the genital mucosa: presentation of viral antigen by DCs to virus-specific Th cells resulted in production of chemokines, which recruited antiviral CTL into the tissue and these cleared the infection. Similar mechanisms might also operate in viral herpes infection of the eye, or in T cell-dependent uveitis. In the support of the latter idea, it has been recently shown that uveal DCs require activation for antigen presentation and that macrophages are immune effectors. The mechanistic link between uveal DCs and macrophages might be Th cells responding to presentation of ocular antigen by producing cytokines and chemokines, which then attract and stimulate other immune effectors, including macrophages, very much like in chronic GN as detailed above. It appears worthwhile to consider intraocular crosstalk between DCs and autoreactive T cells as a progression mechanism in eye disease.