The present invention relates to a monoclonal antibody or fragment thereof that recognizes and binds specifically to beta 1 integrin as an antigen. The present invention also relates to a pharmaceutical composition for preventing or treating cancer including the monoclonal antibody or fragment thereof. The monoclonal antibody of the present invention is useful in preventing or treating cancer due to its ability to inhibit the proliferation and angiogenesis of cancer cells and effectively induce apoptosis

This disclosure relates to methods for enriching a first population of cells positive for a target moiety and/or a second population of cells positive for the target moiety from a sample, wherein a level of the target moiety among the first population of cells is relatively lower than the level of the target moiety among the second population of cells. The methods of this disclosure may also be adapted to assays for determining distinct populations of cells positive for a target moiety in a sample, and to assays for optimizing enrichment conditions. Last, this disclosure relates to kits of components that may be used to carry out the methods and assays.

Disclosed are T-cells that are positive for CD49f and which have an enhanced function compared to CD49f− cells. Methods of isolation of CD49f+ T-cells, as well as compositions and kits thereof are also disclosed. Additionally, enriched CD49f+T-cell populations have an increased proliferative potential, long-term survival and significantly improved efficacy in an adoptive therapeutic setting. The CD49f+ T-cells and CD49f+ T-cell enriched T-cell populations are useful in a range of applications, including for use in treating or inhibiting the development of diseases with immune dysfunction and methods of assessing risk of disease and potential responsiveness in immunotherapy. CD 19 CAR-T cells derived from CD49f+ T-cells and their use in a method of treatment of cancer is also disclosed.

Methods and apparatus for assaying the level of analytes in a sample, related to VLA-4, are disclosed. A method of decreasing the level of an anti-integrin antibody in a subject is described including a) contacting a biological sample from a subject with a detectable capture agent associated with a substrate, wherein the capture agent can bind an anti-integrin antibody in the sample; b) detecting binding of the capture agent with the level of the anti-integrin antibody; and c) treating the subject with plasma exchange until the level of the anti-integrin antibody in the sample reaches a predetermined level.

A method of chronically reducing a patient's pathological inflammation via the administration of an agent that specifically binds to an alpha-4 integrin or a dimer comprising an alpha-4 integrin is disclosed. The agent provided must have a binding affinity such that administration is sufficient to suppress pathological inflammation, and the agent is administered chronically to provide long-term suppression of pathological inflammation.

Methods and apparatus for assaying the level of analytes in a sample, related to VLA-4, are disclosed. A method of decreasing the level of an anti-integrin antibody in a subject is described including a) contacting a biological sample from a subject with a detectable capture agent associated with a substrate, wherein the capture agent can bind an anti-integrin antibody in the sample; b) detecting binding of the capture agent with the level of the anti-integrin antibody; and c) treating the subject with plasma exchange until the level of the anti-integrin antibody in the sample reaches a predetermined level.

The present invention provides the use of the antigens CD49e and/or CD49f as selection markers for enrichment, isolation, detection and/or analysis of atrial and ventricular cardiomyocytes and a method for enrichment, isolation, detection and/or analysis of these cells from a sample comprising cardiomyocytes. In addition substantially pure compositions of these cardiomyocyte subpopulations are provided.

A method of chronically reducing a patient's pathological inflammation via the administration of an agent that specifically binds to an alpha-4 integrin or a dimer comprising an alpha-4 integrin is disclosed. The agent provided must have a binding affinity such that administration is sufficient to suppress pathological inflammation, and the agent is administered chronically to provide long-term suppression of pathological inflammation.

A method of chronically reducing a patient's pathological inflammation via the administration of an agent that specifically binds to an alpha-4 integrin or a dimer comprising an alpha-4 integrin is disclosed. The agent provided must have a binding affinity such that administration is sufficient to suppress pathological inflammation, and the agent is administered chronically to provide long-term suppression of pathological inflammation.

Methods for intervening in conditions of active desmoplasia comprise detecting increased levels of active alpha5-beta-1 integrin and the localization of this active integrin intracellularly away from three dimensional matrix adhesions within the stroma of affected tissues, as well as detecting the concomitant enhanced activity of focal adhesion kinase. Once active desmoplasia is detected, treatments may ensue, which induce a desmoplastic extracellular matrix to revert to a normal/innate phenotype, or which alter the standard of care to improve an outcome that would be less beneficial without the detection of a treatment-impeding desmoplasia condition. Liquid biopsies for detecting active desmoplasia are provided.