Abstract: Methods of treating a disease, disorder or syndrome associated with a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (such as COVID-19) in a subject by administering one or more C-X-C chemokine receptor 3 (CXCR3) antagonist peptides are described. Diagnostic methods for enhancing replication of SARS-CoV-2 in cultured cells and/or detecting the presence of SARS-CoV-2 in cultured cells by contacting the cells with a CXCR3 agonist peptide are also described.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C-X-C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C-X-C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: Administration via inhalation of small peptides that mimic CXCL10 (FIBROKINE™ peptides) is described. The peptides can be administered as an aerosol, such as an aerosol with a droplet size small enough to reach lung alveoli. Use of the peptides to treat fibrosis, such as lung fibrosis, is described.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C—X—C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C-X-C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: Interferon-?-inducible protein 10 (IP-10) peptides, IP-10 peptide variants and in silico designed C—X—C chemokine receptor 3 (CXCR3) peptide agonists are described. The small peptides can be used for inhibiting pathological tissue remodeling and treating fibrosis in a subject, such as a subject with fibrosis of the heart, lung, liver, kidney or skin. The peptide agonists can also be used to treat cardiovascular disease, including myocardial infarction and ischemia-reperfusion injury. Also described are in silico designed peptide antagonists that bind CXCR3 or ligands of CXCR3. These antagonist peptides block CXCR3 signaling by disrupting interaction of CXCR3 with its ligand. Antagonist peptides can be used, for example, to treat myocarditis and atherosclerosis. In additional embodiments agonists and antagonists of CXCR4 are disclosed.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: Described herein is the finding that activators of CXCR3, such as proteins that bind CXCR3 (e.g., IP-9, IP-10 and PF4), enhance the density of goblet cells in the eye. Goblet cells in the conjunctiva are the primary source of tear mucus. Accordingly, the present disclosure describes methods of treating dry eye syndrome by administering an activator of CXCR3. Also described are methods of increasing goblet cells density, such as goblet cell density in the conjunctiva.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3 (CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10) or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of C-X-C chemokine receptor 3(CXCR3). In some embodiments, the activator of CXCR3 is interferon-?-inducible 10 kDa protein (IP-10), or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is platelet factor 4 (PF4) or a fragment or variant thereof.

Abstract: The present disclosure describes methods of treating angiogenic disorders of the eye, such as macular degeneration, restenosis following glaucoma treatment or diabetic retinopathy, by administering an activator of CXCR3. In some embodiments, the activator of CXCR3 is IP-10 or a fragment or variant thereof, such as a fragment comprising or consisting of the C-terminal ?-helix of IP-10. In other embodiments, the activator of CXCR3 is PF4 or a fragment or variant thereof.