At present it is difficult to reconcile these contrasting findings for several reasons: (i) All these models used a similar model (LPS-administration via the airways), yet T-cell deficiency resulted in all possible outcomes, i.e. reduced, similar or increased lung injury; (ii) RAG1−/− and RAG2−/− are thought to possess nearly identical phenotypes [25]; (iii) T-cell dependent changes in TNF levels that have been proposed to explain the increased inflammation seen in γδ-knockout mice, were nearly the same in wt and RAG2−/−mice in the present study [24]. The gene discussed is TNF; the disease is congenital T-cell immunodeficiency.