Abstract: Compositions for treating disorders of iron homeostasis are provided. More particularly, anti-ferroportin antibodies, compositions containing such antibodies, corresponding nucleic acids, vectors and host cells, and methods of making such antibodies are provided.

Abstract: Compositions for treating disorders of iron homeostasis are provided. More particularly, anti-ferroportin antibodies, compositions containing such antibodies, corresponding nucleic acids, vectors and host cells, and methods of making such antibodies are provided.

Abstract: Compositions for treating disorders of iron homeostasis are provided. More particularly, anti-ferroportin antibodies, compositions containing such antibodies, corresponding nucleic acids, vectors and host cells, and methods of making such antibodies are provided.

Abstract: Methods are provided to specifically modulate the trafficking of systemic memory T cells, particularly CD4+ T cells, without affecting naive T cells or intestinal memory T cells. It is shown that systemic memory T cells, which are characterized as CD45Ra?, and integrin ?4?7?, express high levels of CCR4. Ligands of CCR4, such as TARC or MDC, act as an adhesion trigger, wherein upon CCR4 binding, these cells undergo integrin-dependent arrest to the appropriate vascular receptor(s). This arrest acts to localize the cells at the target site. The methods of the invention manipulate this triggering, and CCR4 mediated chemotaxis, to affect the localization of T cells in targeted tissues. In an alternative embodiment, the agent is an antagonist that blocks CCR4 biological activity. An advantage of the invention is the selectivity for systemic memory T cells, without affecting native T cells or intestinal memory T cells.

Abstract: The present invention provides methods of suppressing demyelinating inflammatory disorders in a patient by administering to the patient a compound that inhibits binding of B7RP-1 to ICOS or inhibits signaling through the B7RP-1 pathway. Various therapeutic regimens are provided. Methods of identifying such compounds are also provided. The present invention further provides kits and pharmaceutical compositions useful in the present methods.

Abstract: The present application relates, in part, to methods and compositions for the prevention or amelioration of symptoms of anthrax. In particular, the present invention relates to TANGO 197 and/or TANGO 216 fusion polypeptides and their use as part of such methods.

Abstract: The present application relates, in part, to methods and compositions for the prevention or amelioration of symptoms of anthrax. In particular, the present invention relates to TANGO 197 and/or TANGO 216 fusion polypeptides and their use as part of such methods.

Abstract: The invention relates to antagonists of CX3C chemokine receptor 1 (CX3CR1) function, antagonists of fractalkine function and to therapeutic methods employing the antagonists. The invention also relates to a method for diagnosing rheumatoid arthritis.

Abstract: Methods are provided to specifically modulate the trafficking of systemic memory T cells, particularly CD4+ T cells, without affecting naive T cells or intestinal memory T cells. It is shown that systemic memory T cells, which are characterized as CD45Ra31 , and integrin &agr;4&bgr;731 , express high levels of CCR4. Ligands of CCR4, such as TARC or MDC, act as an adhesion trigger, wherein upon CCR4 binding, these cells undergo integrin-dependent arrest to the appropriate vascular receptor(s). This arrest acts to localize the cells at the target site. The methods of the invention manipulate this triggering, and CCR4 mediated chemotaxis, to affect the localization of T cells in targeted tissues. In one embodiment of the invention, the active agent is a CCR4 agonist, that acts to enhance T cell localization. In an alternative embodiment, the agent is an antagonist that blocks CCR4 biological activity.

Abstract: Methods are provided to specifically modulate the trafficking of systemic memory T cells, particularly CD4+ T cells, without affecting naive T cells or intestinal memory T cells. It is shown that systemic memory T cells, which are characterized as CD45Ra−, and integrin &agr;4&bgr;7−, express high levels of CCR4. Ligands of CCR4, such as TARC or MDC, act as an adhesion trigger, wherein upon CCR4 binding, these cells undergo integrin-dependent arrest to the appropriate vascular receptor(s). This arrest acts to localize the cells at the target site. The methods of the invention manipulate this triggering, and CCR4 mediated chemotaxis, to affect the localization of T cells in targeted tissues. In one embodiment of the invention, the active agent is a CCR4 agonist, that acts to enhance T cell localization. In an alternative embodiment, the agent is an antagonist that blocks CCR4 biological activity.