Abstract: Described herein are methods and compositions for treatment of inflammation, such as inflammation in lung and/or airway tissue, including asthma. Innate lymphoid cells (ILCs), such as type 2 ILC2s, are herein described as capable of IL-33 signaling activation, leading to airway hyperresponsiveness (AHR) and inflammation. Further described is the hereto unknown discovery that ICOS-ligand is expressed in ILC2s, that ICOS binding of ICOS to ICOS-ligand is required for its function in ILC2s, and that while IL-33 treatment induces AHR in control mice, IL-33 cannot induce AHR in mice receiving treatment via anti-ICOS-ligand antibodies. These results suggest new methods and compositions targeting ICOS and ICOS-ligand, such as dual specific antibodies that recognize ICOS and ICOS-ligand, an expression profile unique to ILC2s.

Abstract: Presented herein, in certain embodiments, are compositions comprising a GITR agonist and uses thereof for the treatment of diabetes or related disorders.

Abstract: This disclosure provides methods and compositions for treating diseases and disorders by targeting ILC2s that express the ?7-nicotinic acetylcholine receptor (?7nAChR).

Abstract: Described herein are methods and compositions for treatment of inflammation, such as inflammation in lung and/or airway tissue, including asthma Innate lymphoid cells (ILCs), such as type 2 ILC2s, are herein described as capable of IL-33 signaling activation, leading to airway hyperresponsiveness (AHR) and inflammation. Further described is the hereto unknown discovery that ICOS-ligand is expressed in ILC2s, that ICOS binding of ICOS to ICOS-ligand is required for its function in ILC2s, and that while IL-33 treatment induces AHR in control mice, IL-33 cannot induce AHR in mice receiving treatment via anti-ICOS-ligand antibodies. These results suggest new methods and compositions targeting ICOS and ICOS-ligand, such as dual specific antibodies that recognize ICOS and ICOS-ligand, an expression profile unique to ILC2s.

Abstract: A unique CD4+CD25+ regulatory T cell population develops from naive CD4+CD25? T cells during a TH1 polarized immune response (called TH1-TR cells). These TH1-TR cells can be generated by contacting naïve T cells with mature CD8?+ dendritic cells (DCs) that have been exposed to a TH1 polarizing adjuvant and, in some cases, an antigen of interest. The TH1-TR are identified by their expression of the cytokines IL-10 and IFN-?, the transcriptional regulators T-bet and FoxP3, and the cell surface molecules CD4, CD25, CD69, CD44 and ICOS.

Abstract: This disclosure provides methods for treating asthma or an associated disorder in a patient in need thereof, by administering to the patient an effective amount of an autophagy inducing agent, thereby treating the asthma or the associated disorder. Disorders that can be treated include, allergic asthma, chronic obstructive pulmonary disease, lung inflammation, respiratory tolerance and a lung infection or disorder.

Abstract: This invention discloses an unexpected discovery that plasmacytoid dendritic cells (pDCs) may be segregated into immunogenic or tolerogenic species based on novel biomarkers discovered herein. Exemplary biomarkers include CD8?+?+, CD8?+??, CD8????, C1q, and IL-9R. For example, pDCs with CD8?+?+, CD8?+?? are tolerogenic and CD8???? is immunogenic. Also disclosed are isolated pDCs, compositions comprising the pDCs, methods for isolating the pDCs, methods for treating immune-hyper-reactivity, such as airway hyper-reactivity, food allergy, asthma, and autoimmune disorders, by using compositions containing tolerogenic antigen presenting cells, preferably pDCs disclosed herein. Also disclosed are methods for identifying tolerogenic antigen presenting cells by using one or more novel biomarkers disclosed herein, including RALDH expression, CD8?, CD8?C1qa, C1qc, and IL-9R. Also disclosed are methods for inducing Treg cells by using the pDCs disclosed herein.

Abstract: This disclosure provides methods for treating asthma or an associated disorder in a patient in need thereof, by administering to the patient an effective amount of an autophagy inducing agent, thereby treating the asthma or the associated disorder. Disorders that can be treated include, allergic asthma, chronic obstructive pulmonary disease, lung inflammation, respiratory tolerance and a lung infection or disorder.

Abstract: The present invention is directed to a method of inhibiting allergen-induced airway CD1d activation by administering a composition containing a moiety that blocks CD1d activation. Methods of the invention are useful for treatment and prevention of air-way hyperactivity caused by an allergen, and results in the attenuation of CD1d-restricted immune responses, including treatment of hay fever and asthma are due to air-way hyperactivity, and for systemic administration to attenuate ongoing immune responses. Preferably, these compositions are in a form intended for administration via nasal passages or directly inhaled to the air-ways.

Abstract: A unique CD4+CD25+ regulatory T cell population develops from naive CD4+CD25? T cells during a TH1 polarized immune response (called TH1-TR cells). These TH1-TR cells can be generated by contacting naïve T cells with mature CD8?+ dendritic cells (DCs) that have been exposed to a TH1 polarizing adjuvant and, in some cases, an antigen of interest. The TH1-TR are identified by their expression of the cytokines IL-10 and IFN-?, the transcriptional regulators T-bet and FoxP3, and the cell surface molecules CD4, CD25, CD69, CD44 and ICOS.