Provided herein are methods and compositions for single cell characterization using affinity-oligonucleotide conjugates. Provided herein are methods and compositions for single cell charaterization using tetramer-oligonucleotide conjugates.

There is provided methods of determining tuberculosis (TB) infection status in an individual comprising: (i) providing a sample comprising T-cells; (ii) exposing the sample of (i) to one or more TB antigens; (iii) identifying T-cells in the sample that are CD4 positive and (a) secrete TNF- without secreting IFN-; or (b) secrete IFN- without secreting TNF-; (iv) identifying those cells of (iii) which are also CCR7 and, CD127 negative; and optionally (v) calculating the cells identified in (iv) as a percentage of those identified in (iii); wherein the identification of cells in (iv) and/or the percentage of T-cells calculated in (v) correlates to TB infection status of the individual, and wherein steps (iii) and (iv) can be carried out either sequentially or simultaneously. There are also provided compositions and kits for use in such methods.

Novel complexes of peptides from human collagen type II and types of MHC class II associated with rheumatoid arthritis are provided. There is also provided novel therapies and methods for diagnosis of rheumatoid arthritis.

Methods and kits for evaluating a clinical outcome of an autoimmune disease, specifically disease flare e.g. if the subject stops taking the biologic disease modifying anti-rheumatic drug (DMARD), by comparing biomarkers of CD45RA, TNF-alpha and/or CXCR5 from CD3.sup.+CD4.sup.+ T cell population are disclosed. In a specific embodiment, the ratio of first subset of CD3.sup.+CD4.sup.+CD45RATNFA.sup.+ (memory) T cells to a second subset comprising CD3.sup.+CD4.sup.+CD45RA.sup.+TNFA.sup.+ (nave) T cell is determined, wherein an increase in the ratio indicates a disease flare state of juvenile idiopathic arthritis (JIA). In another embodiment, enrichment of CD45RACR5.sup.+ subset among the T cell population indicates likelihood of flare state in JIA via memory persistence enhancement through B cell interaction. In other embodiments, additional markers including IL-6, CCR6, CD152 and PD1 are also determined, and the enrichment of CD45RA-TNFA.sup.+IL-6.sup.+ subset among the T cell population indicates a likelihood of amplification of the autoimmune disease.

Provided herein are antibodies, or antigen binding portions thereof, that bind to OX40. 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.

The invention provides methods for treating pathological conditions associated with an undesirable inflammatory component. The invention is generally directed to reducing inflammation by administering cells that have one or more of the following effects in an injured subject: interact with splenocytes, preserve splenic mass, increase proliferation of CD4.sup.+ and CD8.sup.+ T-cells, increase IL-4 and IL-10, decrease IL-6 and IL-1, and increase M2:M1 macrophage ratio at the site of injury. The invention is also directed to drug discovery methods to screen for agents that modulate the ability of the cells to have these effects. The invention is also directed to cell banks that can be used to provide cells for administration to a subject, the banks comprising cells having desired potency for achieving these effects.

The present disclosure provides a method of treating cancer by immune checkpoint blockade, or selecting patients for treatment with immune checkpoint blockers, by detecting tumors with high levels of T-lymphocytes with low levels of activation and proliferation. In various embodiments the tissue sample may be from a conventional biopsy. In various embodiments the cancer may be non-small cell lung cancer.

An object of the present invention is to provide an immunopotentiating agent for reducing Tregs (in particular, effector Tregs) and potentiating tumor immunity or infection immunity. Imatinib and/or a salt thereof has the action of reducing Tregs (in particular, effector Tregs) and potentiating tumor immunity or infection immunity, and can be used as an active ingredient for the immunopotentiating agent.

The present disclosure provides methods for measuring the number of CD4+ OX40+ Foxp3+ lymphocytes in a sample containing cancer cells and lymphocytes obtained from a subject by labeling lymphocytes that show CD4 expression in the sample, then labeling lymphocytes that show OX40 expression in the sample, then labeling lymphocytes that show Foxp3 expression in the sample, then measuring the number of CD4+ OX40+ Foxp3+ lymphocytes in the sample. Further provided are methods for determining the prognosis of a subject, predicting responsiveness of a subject having cancer to an OX40 agonist treatment, and methods for treating or delaying progression of cancer based on the number of CD4+ OX40+ Foxp3+ lymphocytes in a sample.

The invention provides compositions, methods, and vaccines that may stimulate the immune system and that may be used for treating malignancies associated with overexpression of the HER3 protein. Such compositions include epitopes of the HER3 protein.