Cell-free compositions for promoting restoration of tissue function or enhancement of tissue function and methods of stimulating or promoting restoration or enhancement of tissue function using the cell-free compositions. The compositions herein help stimulate endogenous pathways via a subject's own cells effectively for improving tissue function, enhancing tissue function, enhancing cell proliferation, etc. The compositions comprise one or a plurality of therapeutic components such as growth factors, extracellular matrix, DNA, RNA, hormones, drugs, cell surface receptors, enzymes, cytokines, angiogenesis modulating factors, etc., e.g., any material that can effectively activation endogenous pathways in the subject's own cell to a desired effect. The cell-free composition comprises a carrier or is attached to or integrated into and/or within a carrier. The carrier may help provide for containment of the therapeutic components and/or provide for time-release of the therapeutic components of the cell-free composition.

The current invention is related to the prevention and treatment of diseases including cancer, autoimmune disease, and infectious disease using CXC chemokines and the receptors to which they agonize. It has been found that certain chemokines, including CXCL4, CXCL9, CXCL10, and CXCL12 have various effects on toll-like receptors in various cell types and these can be utilized for disease treatment and prevention.

Methods of assigning a COVID pathological type for a subject suffering from COVID-19 are provided. Aspects of the methods include assigning a COVID pathological type for the subject based on a determined quantitative, multiplex cytokine/chemokine panel in a test sample from the subject. Also provided are methods of treating a subject (e.g., a long hauler subject) for chronic COVID-19. Aspects of such methods include administering to the long hauler subject a CCR5/CCL5 interaction inhibitor to treat the long hauler subject. Also provided are compositions for use in practicing the methods. The methods and compositions find use in a variety of applications, including patient stratification, treatment and therapy determination and therapy response assessment.

The present invention provides a CXCL12.sub.1 peptide engineered to resist peptide-induced dimerization by maintaining steric repulsion of the chemokine helix, pharmaceutical compositions thereof, and methods of using said dimer in the treatment of cancer, inflammatory disorders, autoimmune disease, and HIV/AIDS.

A composition for influencing biological growth including live cells, a fluid comprising dextrose, a protectant, and a first cytokine having a first concentration within the composition as described within the present disclosure.

The present invention relates to a fusion protein comprising at least two cytokines, of which at least one is a modified cytokine with a strongly reduced binding affinity to its receptor, or to one of its receptors. Preferably, both cytokines are connected by a linker, preferably a GGS linker. The invention relates further to said fusion protein for use in treatment of diseases.

The invention relates to novel Evasin polypeptides with novel chemokine-binding properties and their use in inhibiting chemokines or detecting chemokine expression and inflammation.

The present disclosure is directed to the use of PF4 alone or anti-PF4 antibodies alone or the combination thereof to treat sepsis. Neutrophils release their histone-coated DNA termed neutrophil extracellular traps (NETs) during sepsis and related inflammatory disorders. NETs are broken down and release NET degradation products (NDPs) like histone that are toxic and contribute to the morbidity and mortality in sepsis and related inflammatory disorders. The inventors have shown that a native platelet protein, platelet factor 4 (PF4), which is highly positively-charged, compacts NETs that are in turn highly negatively-charged. These compact NETs are resistant to NDP release and breakdown by circulating DNases. PF4 protects against this lysis and NDP release and improves outcome. The inventors also found that an antibody to PF4 that cross-binds PF4 on NETs further protects against lysis and NDP release. Such antibodies, perhaps supplemented with additional PF4, are therapeutic candidates for treatment of sepsis.

The present disclosure relates to a hypoxia-inducing cryogel, comprising one or more polymer and one or more hypoxia-inducing agent. The present disclosure additionally relates to a hypoxia-inducing construct, comprising a cryogel and a support. Methods of reducing concentration of oxygen in a medium, comprising contacting the medium with a hypoxia-inducing cryogel (HIC) or a hypoxia-inducing construct are disclosed. Additionally, methods of inducing hypoxia in a cell, comprising contacting the cell with a medium, wherein the medium comprises a HIC or a hypoxia-inducing construct are disclosed.

The invention is based on the disclosure provided herein that secondary lymphoid organ chemokine (SLC) inhibits the growth of syngeneic tumors in vivo. Thus, the invention provides a method of treating cancer in a mammal subject by administering a therapeutically effective amount of an SLC to the mammal in combination with a checkpoint inhibitor, including monoclonal antibodies and small molecule inhibitors. Exemplary checkpoint molecules include CTLA-4, a CTLA-4 receptor, PD-1, PD1-L1, PD1-L2, 4-1BB, OX40, LAG-3, TIM-3 or a combination thereof. SLCs useful in the methods of the invention include SLC polypeptides, variants and fragments and related nucleic acids.