Abstract: The present disclosure provides, inter alia, methods of treating a solid-tumor by administering an effective amount of a Chemokine Receptor 2 (CCR2) antagonist. Also provided herein are methods of reducing the number of macrophages in a solid tumor microenvironment, said method comprising administering effective amount of a Chemokine Receptor 2 (CCR2) antagonist. In an additional aspect, the current disclosure further provides methods of increasing the number CD8+ T cells in a solid tumor microenvironment, said method comprising administering effective amount of a Chemokine Receptor 2 (CCR2) antagonist.

Abstract: The present disclosure provides, inter alia, methods of treating generalized pustular psoriasis (GPP) by administering an effective amount of a Chemokine Receptor 6 (CCR6) antagonist and/or a C-X-C motif chemokine receptor 2 (CXCR2) antagonist. Also provided herein are methods of modulating dysregulated IL-36 signaling in a subject in need thereof and methods of reducing neutrophil, inflammatory dendritic cell (iDC), and/or CD4 T cell accumulation in a subject in need thereof, said methods, include dministering an effective amount of a Chemokine Receptor 6 (CCR6) antagonist and/or a C-X-C motif chemokine receptor 2 (CXCR2) antagonist.

Abstract: Provided herein are methods of treating cancer in an individual in need thereof, the methods comprising administering to the individual a CXCR7 inhibitor. In some embodiments, additional therapeutic agents are used. Also provided herein are methods of preventing precancerous cells expressing FRS2? from developing into cancer, the method comprising administering to an individual having precancerous cells expressing FRS2? a CXCR7 inhibitor. In some embodiments, additional therapeutic agents are used.

Abstract: The present disclosure is drawn to the combination therapy of a Chemokine Receptor 2 (CCR2) antagonist and a PD-1 and/or PD-L1 inhibitor in the treatment of cancer.

Abstract: The present disclosure provides, inter alia, methods of treating generalized pustular psoriasis (GPP) by administering an effective amount of a Chemokine Receptor 6 (CCR6) antagonist and/or a C—X—C motif chemokine receptor 2 (CXCR2) antagonist. Also provided herein are methods of modulating dysregulated IL-36 signaling in a subject in need thereof and methods of reducing neutrophil, inflammatory dendritic cell (iDC), and/or CD4 T cell accumulation in a subject in need thereof, said methods, include administering an effective amount of a Chemokine Receptor 6 (CCR6) antagonist and/or a C—X—C motif chemokine receptor 2 (CXCR2) antagonist.

Abstract: The present disclosure provides, inter alia, methods of treating a solid-tumor by administering an effective amount of a Chemokine Receptor 2 (CCR2) antagonist. Also provided herein are methods of reducing the number of macrophages in a solid tumor microenvironment, said method comprising administering effective amount of a Chemokine Receptor 2 (CCR2) antagonist. In an additional aspect, the current disclosure further provides methods of increasing the number CD8+ T cells in a solid tumor microenvironment, said method comprising administering effective amount of a Chemokine Receptor 2 (CCR2) antagonist.

Abstract: Provided herein are compositions, methods and kits for treating inflammatory bowel disease (IBD) such as Crohn's disease and ulcerative colitis in a mammal in need thereof. The method include administering to a subject with IBD a combination therapy containing a therapeutically effective amount of a chemokine receptor 9 (CCR9) inhibitor compound and a therapeutically effective amount of an anti-?4?7 integrin antibody such as vedolizumab. Also provided herein is a kit containing the CCR9 inhibitor compound and anti-?4?7 integrin antibody.

Abstract: Provided herein are compositions, methods and kits for treating inflammatory bowel disease (IBD) such as Crohn's disease and ulcerative colitis in a mammal in need thereof. The method include administering to a subject with IBD a combination therapy containing a therapeutically effective amount of a chemokine receptor 9 (CCR9) inhibitor compound and a therapeutically effective amount of an anti-TNF? antibody. Also provided herein is a kit containing the CCR9 inhibitor compound and anti-TNF? antibody.

Abstract: Precharging systems and methods are presented for precharging a DC bus circuit in a power conversion system, in which precharging current is connected through a precharging resistance coupled between only a single AC input line and the DC bus circuit when the DC bus voltage is less than a non-zero threshold, and a controller individually activates controllable rectifier switching devices when the DC bus voltages greater than or equal to the threshold using DC gating or pulse width modulation to selectively provide a bypass path around the precharging resistance for normal load currents in the power conversion system.

Abstract: Precharging systems and methods are presented for precharging a DC bus circuit in a power conversion system, in which precharging current is connected through a precharging resistance coupled between only a single AC input line and the DC bus circuit when the DC bus voltage is less than a non-zero threshold, and a controller individually activates controllable rectifier switching devices when the DC bus voltages greater than or equal to the threshold using DC gating or pulse width modulation to selectively provide a bypass path around the precharging resistance for normal load currents in the power conversion system.

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: 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.

Abstract: A rectangular waveguide housing and a waveguide radiator have coaxial cavities that are contiguous. A pair of perpendicular walls intersect substantially on the axis of the housing to form therein four similar rectangular subwaveguides that may be excited to propagate electromagnetic waves in a TE.sub.10 mode. The walls have edges that are in the boundary between the contiguous cavities. A pair of intersecting tabs extend from the edges into the radiator. Additionally, a protrusion extends within the radiator from the intersection of the tabs. The polarities of the waves in the subwaveguides are selected to cause an electromagnetic wave to propagate through the radiator in either of two orthogonal difference modes or a sum mode that has desired beam shaping properties. The protrusion causes one of the difference modes to have a desired polarization.