The present invention relates to methods for determining, modulating or adjusting a treatment regimen with a chemotherapeutic agent in a patient affected with a cancer.

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-α without secreting IFN-γ; or (b) secrete IFN-γ without secreting TNF-α; (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.

Immune context scores are calculated for stage IV colorectal tumor tissue samples using non-continuous scoring functions. Feature metrics for at least one immune cell marker are calculated for a region or regions of interest, the feature metrics including at least a density of human CD8+ cells in a region of interest including a tumor core to generate an immune context score. The immune context score can then be used as a predictive metric (e.g. likelihood of response to a particular treatment course). The immune context score may then be incorporated into diagnostic and/or treatment decisions.

T cell surface marker, CRTH2, is a target for treating Postural Orthostatic Tachycardia Syndrome, a hemodynamic abnormality. Targeting CRTH2 permits control of disease symptoms in POTS, for which no FDA approved treatment is currently available. Cell surface expression on certain T cell subsets characterizes the syndrome. Cell surface expression can be conveniently determined in plasma samples using flow cytometry.

There is provided a method of evaluating risk of severe outcome of an infectious disease and/or an inflammatory disease in a patient, the method comprising: determining/measuring the number of one or more immune cells selected from the group consisting of VD2 T cells, CD8 T cells, and immature neutrophils in a sample obtained from the patient, wherein the patient has an enhanced risk of severe infectious disease and/or inflammatory disease outcome when: (i) the ratio of immature neutrophils to VD2 T cell is at least 2:1, and/or (ii) the ratio of immature neutrophils to CD8 T cell is at least 0.5:1. Also disclosed are method of treating a patient with a severe infectious disease and/or inflammatory disease and kit for use in methods thereof.

Provided herein am compositions and methods for characterizing and treating neurodegenerative disease. In particular, provided herein are compositions and methods for measuring T cell markers associated with Alzheimer's disease.

Compositions and methods for fluorescence activated cell analysis of blood cell populations.

The disclosure provides, inter alia, breast cancer biomarkers, methods of detecting exhausted CD8+ T cells in breast cancer patients, methods of detecting CD26+CD4+ T cells in breast cancer patients, methods of treating breast cancer patients, and methods of identifying risk outcomes for breast cancer patients.

This invention relates, at least in part, to compositions comprising synthetic nanocarriers and immunosuppressants that result in immune suppressive effects. Such compositions can further comprise antigen and provide antigen-specific tolerogenic immune responses.

Prolonged exposure of CD8.sup.+ T cells to antigenic stimulation leads to a state of diminished function, termed exhaustion; during exhaustion there is a subset of functional CD8.sup.+ T cells defined by surface expression of SIRP(alpha) protein. On SIRP.sup.+ CD8.sup.+ T cells, expression of coinhibitmy receptors is counterbalanced by expression of co-stimulatory receptors and it is only these SIRP.sup.+ cells that actively proliferate, transcribe IFNg and show cytolytic activity. Therapeutic blockade of PD-L1 or other inhibitory receptors to reinvigorate exhausted CD8.sup.+ T cells expands the cytotoxic subset of SIRP.sup.+ CD8.sup.+ T cells.