The present invention includes methods for treating, preventing, or assessing the levels of risk for acute kidney injury (AKI) in a subject via measuring concentrations of tumor necrosis factor receptor-1 (TNFR1), tumor necrosis factor receptor-2 (TNFR2), and kidney injury molecule-1 (KIM-1).

Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce the antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.

Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce the antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.

Provided herein is a reporter system for identifying a cytokine receptor modulator and uses thereof.

Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.

A receptor is provided having a heterologous binding site that activates, when bound, a signaling domain related to the TNF receptor superfamily. Methods/uses of the foregoing in whole cell biosensors are also provided. There is also provided a library comprising a plurality of unique biosensor cells for binding unknown binding substrates. Each unique biosensor is a host cell having a receptor which signals production of a positive selectable marker and/or a negative selectable marker in response to the receptor being bound. Also provided is a method of identifying biosensor cells from a library that is specifically activated by a target, involving (a) contacting the library with the target substrate under positive selection conditions; (b) contacting the library with a control substrate under negative selection conditions; and (c) identifying biosensor cells which survive (a) and (b) as biosensor cells which are specifically activated by the target.

The present disclosure relates to a method for detecting and/or quantifying expression of at least a first cell surface moiety and of a second cell surface moiety in a patient sample, and to a method for detecting and/or quantifying clustering of at least a first cell surface moiety with a second cell surface moiety in a sample, wherein the sample is exposed to a molecule having binding specificity for the at least first and second cell surface moieties. The present disclosure further relates to a method for predicting the responsiveness of a subject to such binding molecule, a method for determining the effectiveness of such binding molecule, a method for confirming the mode of action of such binding molecule, a method for treating a subject, and a method for screening one or more test agents for the ability to induce clustering of a first cell surface moiety with a second cell surface moiety.

Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce the antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.

Two patients diagnosed with KLS were treated. One patient had severe KLS that progressed to the equivalent of pediatric Kawasaki Disease Shock Syndrome (KDSS). The second patient had a typical KLS presentation and clinical course. Cytokines and chemokines provide inflammatory signatures in the serum that reflect the polarity of the immune response and the affected cell types. Multiplex ELISA technology was used to define the cytokine milieu in the serum of the two adult HIV patients with KLS during the acute and convalescent phases. Those sera were compared with sera from asymptomatic HIV subjects and a normal serum control. Those comparisons suggest that HIV KLS is a dysfunctional Th2 response to an unknown inciting agent in the vascular wall, and that a multiplex ELISA or similar technology based a limited combination of KLS/KD pathogenesis-related cytokines (IL-6, IL-13, sTNFRII) and endothelial/smooth muscle chemokines (CCL1, CCL2, CxCL11) may provide an objective tool for diagnosing KLS and Kawasaki Disease. Because KD and HIV KLS are the only known Th2 vasculitidies that spare the lungs (unique clinical presentation) and include plasma cell infiltration of the vascular wall as a prominent histopathologic feature (unique pathophysiology), a diagnostic test based on combinations of the above analytes will be highly specific and therefore clinically useful.

Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce the antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.