The present invention provides methods, assays and kits for assessment of patients positive for SARS-CoV-2 infection and methods of diagnosis and treatment of COVID-19 disease and for assessment and evaluation of individuals prior to vaccination with live attenuated virus vaccines, particularly including yellow fever vaccines and COVID-19 vaccines, to assess risk for vaccine-associated disease and adverse events, and for evaluation, treatment and management of patients who develop vaccine-associated disease. The invention provides methods and assays for identification and characterization of inborn errors of type I interferon immunity and also auto-antibodies against Type I IFNs that are associated with severe COVID-19 disease or that are correlated and linked with vaccine-associated disease. The invention further provides methods of diagnosing and determining altered response to or susceptibility to SARS-CoV-2 infection or to live attenuated virus vaccines and for applicable and suitable treatment of COVID-19 disease or vaccine-associated disease.

The present invention relates to methods for selecting and treating patients with active Systemic Lupus Erythematosus (SLE) that are predicted to have an increased likelihood of having a positive response to a treatment with a safe and effective amount of an anti-IL-12/IL-23p40 antibody or an anti-IL-23 antibody, e.g., informs on what patients to treat with an anti-IL-12/IL-23p40 antibody.

Disclosed herein are methods of determining innate immune response to infections of a subject comprising mixing a subject blood sample comprising plasma with an anticoagulant solution; adding a sample of innate immune cells incubated with one or more stimulants to the mixture to form a cell sample aliquot; incubating the cell sample aliquots with and without the stimulants for at least one hour at an optimal temperature; separating the plasma from the innate immune cells in the aliquot; measuring one or more cytokines in the plasma; calculating a net stimulation of cytokines the cell sample aliquot; and comparing the net stimulation to a reference group of subjects having adequate innate immunity reactivity. Also disclosed are methods of treating a subject having an innate immune response to an infection.

An exemplary embodiment of the present disclosure provides a composition comprising two or more cytokines, and one or more of keratan sulfate, chondroitin sulfate, or hyaluronic acid. The composition can simulate a fluid from a patient. The simulated fluid has a viscosity, a storage modulus, and a loss modulus similar to that of patient-derived synovial fluid. A method for making a composition for simulating a fluid from a patient is also disclosed. The method includes creating a mixture comprising two or more cytokines, and one or more of keratan sulfate, chondroitin sulfate, or human serum albumin. The method also includes adding a low molecular weight hyaluronic acid to the mixture, adding a high molecular weight hyaluronic acid to the mixture, and incubating the mixture for a predetermined time at a temperature ranging from approximately 0° C. to approximately 10° C.

Methods and compositions are provided for assessing antigen presentation and potency of Listeria-based immunotherapeutics in inducing an immune response.

The invention relates to materials, methods and devices useful for sampling biological molecules, including biomarkers and/or metabolites. In particular, the invention relates to surface functionalised xerogels and surface functionalised poly(dimethyl) siloxane (PDMS), devices comprising those materials, and methods of using the materials and devices for sampling, analysing or detecting biological molecules.

Disclosed are methods of treating individuals with yeast-based immunotherapy who have been preselected as being sensitive to type I interferons, as well as methods for selecting individuals for treatment with yeast-based immunotherapeutic compositions and methods for enhancing or improving an individual's response to yeast-based immunotherapy, based on the individual's sensitivity to type 1 interferons (T1IFNs).

An antibody binding to IPC was obtained by using an animal cell in which a cell membrane protein associatable with ILT7 was co-expressed as an immunogen. The antibody of the invention has a high specificity which allows immunological distinction between other ILT family molecules and ILT7. The anti-ILT7 antibody of the invention bound to IPC and inhibited the activity thereof. With the anti-ILT7 antibody of the invention, the IPC activity can be inhibited and an interferon-related disease can be treated or prevented. ILT7 expression is maintained even in IPC in the presence of IFN. Therefore, an inhibitory action of IPC activity by the anti-ILT7 antibody can be expected even in an autoimmune disease patient with an increased production of IFN.

Disclosed are methods of treating individuals with yeast-based immunotherapy who have been preselected as being sensitive to type I interferons, as well as methods for selecting individuals for treatment with yeast-based immunotherapeutic compositions and methods for enhancing or improving an individual's response to yeast-based immunotherapy, based on the individual's sensitivity to type 1 interferons (T1IFNs).

A novel IFN-/ independent ligand receptor system which upon engagement leads, among other things, to the establishment of an anti-viral state is disclosed. Further disclosed are three closely positioned genes on human chromosome 19 that encode distinct but highly homologous proteins, designated IFN-1, IFN-2, IFN-3, based inter alia, in their ability to induce antiviral protection. Expression of these proteins is induced upon viral infection. A receptor complex utilized by all three IFN- proteins for signaling is also disclosed. The receptor complex is generally composed of two subunits, a novel receptor designated IFN-R1 or CRF2-12, and a second subunit, IL-10R2 or CRF2-4, which is also a shared receptor component for the IL-10 and IL-22 receptor complexes. The gene encoding IFN-R1 is generally widely expressed, including many different cell types and tissues. Expression of these proteins is induced by immune events, including, for example, upon viral infection. Apoptotosis may also be induced under effective conditions.