Nature Immunology pp 965 - 973, pp 974 - 981 and pp 982 - 990

T cells must find their way to sites of infection or inflammation to mediate an effective immune response. In the October issue of Nature Immunology, scientists have discovered how T cells home to problem areas in the body.

Three groups have now found that the lipid leukotriene B4 (LTB4) is a major mediator of the migration of 'effector' T cells. The recruitment of CD4⁺ and CD8⁺ effector T cells to the inflamed site early in the response requires LTB4. This lipid is most likely released by activated mast cells (one of the 'sentinel cells' of the tissue's early warning system) and other leukocytes that reside in the inflamed tissues. Although further work will be required to establish the applicability of these findings to clinical settings, pharmacological inhibition of LTB4 could prove useful for inhibiting recruitment of pathogenic effector cells in inflammatory diseases.

Nature Immunology pp 957 - 964

Defective T cell responses are a common feature of patients with certain infectious diseases, autoimmune disorders and cancers that differ widely in their causes and symptoms. In the October issue of Nature Immunology scientists have now identified persistent infection as the major factor linking these diverse pathologies.

Michal Baniyash and colleagues from Hebrew University, Israel, hypothesized that persistent exposure to antigen could account for the impaired T cell responses observed in different diseases. Animals persistently exposed to bacteria had poor T cell responses—examination of the T cell receptor complex showed defective zeta chain expression on the cell surface. Importantly, chronic bacterial infection reduced the ability of the animal to fight influenza infection. The authors hypothesize that zeta chain down-regulation could be a physiological mechanism that helps prevent overblown immune responses. However, it can act as a double-edged sword by impairing the ability to respond adequately to chronic diseases.