We study the Makran subduction zone, along the southern coasts of Iran and Pakistan, to gain insights into the kinematics and dynamics of accretionary prism deformation. By combining techniques from seismology, geodesy and geomorphology, we are able to put constraints on the shape of the subduction interface and the style of strain across the prism. We also address the long-standing tectonic problem of how the right-lateral shear taken up by strike-slip faulting in the Sistan Suture Zone in eastern Iran is accommodated at the zone's southern end. We find that the subduction interface in the western Makran may be locked, accumulating elastic strain, and move in megathrust earthquakes. Such earthquakes, and associated tsunamis, present a significant hazard to populations around the Arabian Sea.

SummarySeveral autoimmune diseases, mainly autoantibody-mediated, are attenuated by infusion of total IgG (IVIg). The efficacy varies widely from one patient to another. Using an experimental model of in vitro phagocytosis of autoantibody-coated erythrocytes by mouse macrophages, we analysed the possible causes for such a variability. Our results indicated that the efficacy of the phagocytosis inhibition depends upon different factors, such as the isotype and the extent of polymerization of the immunoglobulin used for the treatment as well as the genetic background of the mice and the state of macrophage activation that can be influenced by concomitant viral infection. The development of an in vitro assay for the phagocytic activity of macrophages might improve the selection of patients susceptible to benefit from IVIg treatment.

Summary Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of this situation is underscored by the emergence of new potentially human pathogenic influenza strains, avian H5N1 being the most recent example. We present evidence that antibodies against T cell immunoglobulin mucin‐1 (TIM‐1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross‐strain immune reactivity. To determine potential immunostimulatory properties of anti‐TIM‐1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM‐1‐specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen‐specific lymphocyte proliferation and cytokine production. Results show that TIM‐1 antibodies enhance antigen‐specific cellular proliferation (P < 0·05) and interferon (IFN)‐γ production (P < 0·01). Using blocking anti‐CD4 and CD8 antibodies, it was observed that antigen‐specific cellular proliferation is CD4‐dependent and that the majority of proliferating cells are CD4+. Finally, vaccination with inactivated influenza virus with TIM‐1 antibody results in the significant (P < 0·001) induction of proliferation and IFN‐γ production upon stimulation with one of three serologically distinct strains. TIM‐1 antibodies demonstrate an adjuvant effect promoting antigen‐specific cellular proliferation and IFN‐γ production, which are important for the promotion of cell‐mediated immunity. These results are the first to suggest that TIM‐1 antibody may serve as a potent adjuvant in the development of new influenza virus vaccines.