Compositions comprising one or more phytocannabinoids and methods of use thereof for treatment of cancer, immune modulation, and protecting the immune system are provided.

Compositions comprising one or more phytocannabinoids and methods of use thereof for treatment of cancer, immune modulation, and protecting the immune system are provided.

The present invention relates to compositions and methods utilizing anti-TNF antibodies or antigen binding fragments thereof in a treatment of active Ankylosing Spondylitis (AS), e.g., a treatment utilizing the anti-TNF antibody having heavy chain complementarity-determining region (CDR) amino acid sequences SEQ ID NOS:40-42 and light chain CDR amino acid sequences SEQ ID NOS:43-45.

The present invention relates to compositions and methods utilizing anti-TNF antibodies or antigen binding fragments thereof in a treatment of active Ankylosing Spondylitis (AS), e.g., a treatment utilizing the anti-TNF antibody having heavy chain complementarity-determining region (CDR) amino acid sequences SEQ ID NOS:40-42 and light chain CDR amino acid sequences SEQ ID NOS:43-45.

This disclosure provides methods of making a megakaryocyte-erythroid progenitor cell (MEP), comprising differentiating a MEP precursor cell into a MEP in culture in the presence of an aryl hydrocarbon receptor (AhR) modulator. In some embodiments the AhR modulator is an AhR antagonist. In some embodiments the AhR modulator is an AhR agonist. In some embodiments the methods comprise culturing MEP precursor cells in the presence of an AHR antagonist and then culturing MEP precursor cells in the presence of an AHR agonist. In some embodiments the stem cell is a pluripotent stem cell. In some embodiments the MEP co-expresses CD41 and CD235. In some embodiments the number of MEPs produced in the culture increases exponentially. Methods of making a red blood cell (RBC) by culturing a MEP in the presence of an AhR modulator are also provided. Methods of making a megakaryocyte and/or a platelet, comprising culturing a MEP in the presence of an AhR modulator are also provided. In some embodiments the AhR modulator is an AhR antagonist. This disclosure also provides compositions comprising at least 1 million MEPs per ml and compositions in which at least 50% of the cells are MEPs, among other things.

This disclosure provides methods of making a megakaryocyte-erythroid progenitor cell (MEP), comprising differentiating a MEP precursor cell into a MEP in culture in the presence of an aryl hydrocarbon receptor (AhR) modulator. In some embodiments the AhR modulator is an AhR antagonist. In some embodiments the AhR modulator is an AhR agonist. In some embodiments the methods comprise culturing MEP precursor cells in the presence of an AHR antagonist and then culturing MEP precursor cells in the presence of an AHR agonist. In some embodiments the stem cell is a pluripotent stem cell. In some embodiments the MEP co-expresses CD41 and CD235. In some embodiments the number of MEPs produced in the culture increases exponentially. Methods of making a red blood cell (RBC) by culturing a MEP in the presence of an AhR modulator are also provided. Methods of making a megakaryocyte and/or a platelet, comprising culturing a MEP in the presence of an AhR modulator are also provided. In some embodiments the AhR modulator is an AhR antagonist. This disclosure also provides compositions comprising at least 1 million MEPs per ml and compositions in which at least 50% of the cells are MEPs, among other things.

The present disclosure provides materials and methods for reducing inflammation in the gut and/or joints of a patient, and optionally treating rheumatoid arthritis (RA) and other inflammatory or autoimmune diseases, in a patient. The present disclosure provides such methods based, in part, on the susceptibility of the patient's gut microbiome to methotrexate (MTX) as described herein.

The present disclosure provides materials and methods for reducing inflammation in the gut and/or joints of a patient, and optionally treating rheumatoid arthritis (RA) and other inflammatory or autoimmune diseases, in a patient. The present disclosure provides such methods based, in part, on the susceptibility of the patient's gut microbiome to methotrexate (MTX) as described herein.

A cosmetic method for modulating pigmentation in a subject includes administering a modulator of angiotensin-converting enzyme 2 (ACE2 modulator) to the subject. The ACE2 modulator can be an inhibitor of angiotensin-converting enzyme 2 (ACE2 inhibitor), in which case, the ACE2 inhibitor can be administered to increase pigmentation in the subject. The ACE2 modulator can also be an activator of angiotensin-converting enzyme 2 (ACE2 activator), in which case the ACE2 activator can be administered to decrease pigmentation in the subject. The treatment of inflammatory skin disease can also be achieved by inhibition of angiotensin-converting enzyme 2.

A cosmetic method for modulating pigmentation in a subject includes administering a modulator of angiotensin-converting enzyme 2 (ACE2 modulator) to the subject. The ACE2 modulator can be an inhibitor of angiotensin-converting enzyme 2 (ACE2 inhibitor), in which case, the ACE2 inhibitor can be administered to increase pigmentation in the subject. The ACE2 modulator can also be an activator of angiotensin-converting enzyme 2 (ACE2 activator), in which case the ACE2 activator can be administered to decrease pigmentation in the subject. The treatment of inflammatory skin disease can also be achieved by inhibition of angiotensin-converting enzyme 2.