The present invention encompasses compositions and methods useful to treat or prevent Clostridium difficile antibiotic-associated colitis through administration of IL-25 and/or downstream cytokines IL-13, IL-4, and IL-5. It is disclosed herein that IL-25 expression is decreased during antibiotic treatment and during bacterial infection and that treatment with IL-25 protein is protective during infection. It is further disclosed herein the unexpected result that IL-25 treatment protects against C. difficile-associated mortality and morbidity. The present application further describes an unexpected result regarding eosinophils and their role in combating infection and their relationship to the effectiveness of IL-25.

Provided herein is technology relating to predicting a subject's resistance or responsiveness to a decitabine based therapy and particularly, but not exclusively, to methods, compositions, and related uses for predicting a subject's resistance or responsiveness to a decitabine based therapy wherein the subject is diagnosed with chronic myelomonocytic leukemia.

Methods of selecting test compounds on the basis of their cellular response profiles are disclosed. For a given test compound, a cellular response is determined by introducing into an array of individually addressable microwells a population of cells comprising a plurality of cell types and contacting the cells with the test compound. The cellular response profile for the test compound is then compared to a desired cellular response profile, and the test compound is selected based on the comparison.

Methods for treating cancer, e.g., in conjunction with anti-cancer therapy, like immunotherapy, and for identifying candidate therapeutic agents, by targeting ICAM4. While MDSCs in mice have been extensively characterized, their human counterparts are not well defined, and cell markers present in mice are not always usable in humans. MDSCs have been described as a heterogenous population of myeloid derived cells with immune suppressive capacity (5, 9, 40, 41). Recent renewed interest in the role of MDSC accumulation in human tumors has resulted in the increased need to define these cells better in order to target them for therapeutic intervention.

The invention provides in vivo methods for identifying cancer-associated immunotherapy targets.

The methods and kits described herein are based, in part, to the discovery of a phenotype representing a fully-reprogrammed iPS cell and several reprogramming intermediates. The methods and kits described herein permit identification of fully-reprogrammed iPS cells and further permits one of skill in the art to monitor the emergence of iPS cells during the reprogramming process. The methods/kits can also be performed using real time using live cell imaging. Also described herein are methods for screening candidate reprogramming agents by monitoring the emergence of fully-reprogrammed iPS cells in the presence and absence of such an agent.

Innate lymphoid cells (ILCs) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC precursors (ILCP). Still, how ILCP relate to mature tissue-resident ILCs remains unclear. ILCP that are present in the blood and all tested lymphoid and non-lymphoid human tissues were identified. Human ILCP fail to express the signature transcription factors (TF) and cytokine outputs of mature NK cells and ILCs but are epigenetically poised to do so. Human ILCP robustly generate all ILC subsets in vitro and in vivo. While human ILCP express RAR related orphan receptor C (RORC), circulating ILCP can be found in RORC-deficient patients that retain potential for EOMES.sup.+ NK cells, T-BET.sup.+ ILC1, GATA-3.sup.+ ILC2 and for IL-22.sup.+ but not for IL-17A.sup.+ ILC3. A model of tissue ILC differentiation (‘ILC-poiesis’) is proposed whereby diverse ILC subsets are generated in situ from ILCP in response to environmental stressors, inflammation and infection.

The present invention relates to a pharmaceutical composition for treating a cancer or an infection in a subject by administrating an amount of an IL-15 derivative conjugate so as to induce a proliferation of natural killer cells (NK cells) which is the same or higher than the one obtained with high dose of interleukin-2 (HDIL-2); eventually associated with a pharmaceutically acceptable carrier.

The presently disclosed subject matter provides methods for determining the propensity of a composition, e.g., a composition comprising an antibody or a fragment thereof, to elicit production of anti-drug antibodies (ADAs) and kits for performing such methods.

The present disclosure an in vitro method of assaying the stimulation of a cytokine storm response comprising the steps of: a. co-culturing PBMCs and matched differentiated endothelial cells to provide a system representative of human responses in vivo, and b. exposing the co-cultured cell system to a test agent, c. analyzing the system for the presence of one or more cytokines released after exposing the co-culture system to said test agent, and d. optionally evaluating the response to the test agent in comparison to a response to one or more control agents.