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This technology includes a cell line secreting an IgG monoclonal antibody to mouse ZP2 which is useful to detect mouse ZP2 on immunoblot, immunohistology and immunoprecipitation, and prevents female fertility if administered IP in mice.

This technology includes a cell line to be used for the study of anti-psychotic therapies and potentially Parkinson’s disease. Activation of D1 dopamine receptors plays a critical role in many fundamental CNS processes. M4 mAChRs are coexpressed with D1 dopamine receptors in a specific subset of striatal medium spiny neurons that contain GABA as the major neurotransmitter. The present study used Cre/LoxP technology to generate mutant mice that lack M4-¬-AChRs only in D1 dopamine receptor-¬-expressing cells to investigate the physiological relevance of mAChRs in this neuronal subpopulation.

This technology includes an immunoassay to measure SARS-CoV-2 antibodies against the nucleocapsid and spike proteins.

Local inflammation processes are crucially important in the host defense against pathogens and for successful immunization because proinflammatory cytokines are necessary for initiation and propagation of an immune response. However, normal inflammatory responses are eventually terminated by physiological termination mechanisms, thereby limiting the strength and duration of immune responses, especially to weak antigens. The inventors have shown that adenosine A2a and A3a receptors play a critical role in down-regulation of inflammation in vivo.

Patient conditioning is a critical initial step in hematopoietic stem and progenitor cell (HSPC) transplantation procedures to enable marrow engraftment of infused cells. Conditioning regimens have traditionally been achieved by delivering cytotoxic doses of chemotherapeutic agents and radiation. However, these regimens are associated with significant morbidity and mortality, and cannot be used safely in elderly or subjects with comorbidities.

This technology includes a strategy to target tumor cells that lost antigen following reaction with a therapeutic antibody by targeting the complement component C3d that has been deposited on target cells by the primary antibody. We previously generated a C3d-specific mouse/human chimeric antibody called C8xi and obtained proof of principle for the approach in two preclinical models. Here we summarize the generation of a new set of C3d targeting antibodies.

The present invention discloses a method of enhancing progenitor cell differentiation, including enhancing myogenesis, neurogenesis and hematopoiesis, by contacting a progenitor cell with an effective amount of a deacetylase inhibitor (DI). The progenitor cell can be part of cell culture, such as a cell culture used for in vitro or in vivo analysis of progenitor cell differentiation, or can be part of an organism, such as a human or other mammal.

A human mast cell line LAD2 that more closely resembles normal in vivo and in vitro human mast cells by expressing functional FcepsilonRI receptors and responding to stem cell factor (SCF) with proliferation, as described in Leuk Res. 2003 Aug;27(8):677-82 and developed by the laboratory of Dr. Dean Metcalfe at the National Institute of Allergy and Infectious Diseases.  This cell line also releases mediators by cross-linking FcgammaRI (CD64) receptors and express FcgammaRII (CD32).

The ubiquitous use of antibiotics has resulted in the selection of bacteria that are relatively resistant to these drugs. Furthermore, few drugs are effective against viral and fungal microorganisms. There is therefore a continuing need to identify novel agents that reduce or inhibit the growth of such microorganisms, or to identify ways of modifying existing agents in order to give them superior antimicrobial activities, or to identify agents that may recruit inflammatory cells.

Tumor Necrosis Factor alpha (TNF-alpha) is a multifunctional cytokine that mediates inflammation, immune regulation, and cellular proliferation. This cytokine is converted to its active form by TNF-alpha converting enzyme (TACE). Pathological increases in TNF-alpha activity have been associated with a wide variety of inflammatory diseases, including inflammatory bowel disease, rheumatoid arthritis, and cancer. Inhibiting the conversion of TNF-alpha to its active form by inhibiting TACE represents a potential treatment for these diseases.