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Immune checkpoint inhibitors (e.g. CTLA-4, PD-L1) have recently shown significant promise in the treatment of cancer.  However, when used alone, these checkpoint inhibitors are limited by the absence or repression of immune cells within the targeted cancer.  For those cancers associated with these limited immune systems, there remains a need for effective therapies.  Agents capable of recruiting and activating immune cells to these types of cancers could extend the overall and complete response rates of combination therapies within the immunooncology domain. 

HMGN polypeptides belong to the high mobility group (HMG) family of chromosomal binding peptides. HMGN polypeptides typically function inside the cell nucleus to bind to DNA and nucleosomes and regulate the transcription of various genes. HMGN polypeptides also can be released by peripheral blood mononuclear cells. However, the extracellular release of a HMGN polypeptide initiates activation of the immune system. Therefore, it has potential use as a biological therapeutic for stimulating an immune response.

The National Cancer Institute's Molecular Targets Development Program is seeking parties interested in collaborative research to further develop, evaluate, or commercialize cancer inhibitors isolated from the African plant Phyllanthus englerii. The technology is also available for exclusive or non-exclusive licensing.

Bone-loss-related diseases, such as periodontitis, are characterized by an imbalance between the formation and activity of osteoblasts and osteoclasts, leading to bone loss. There are several signaling pathways that participate in the osteoclastogenesis process. Finding inhibitors of these pathways and other osteoclastogenesis-related pathways may have an effect on bone-loss diseases.

Currently available topical antibiotic formulations effectively eliminate bacteria at a wound site. Eliminating bacteria in the wound also eliminates the molecular signals present in bacterial DNA that stimulate the immune system's wound healing processes. Without these signals, the rate of wound healing is diminished.  

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths in developed countries.  Despite the availability of several synergistic, targeted therapy regiments, the 5-year survival rate for NSCLC is only 15%.  The poor prognosis of NSCLS is due in part to limitations of current treatments, which do not trigger an immune response against NSCLC, nor can they be directly delivered into the lungs.  

Tumor-specific mutated proteins can create neoepitopes, mutation-derived antigens that distinguish tumor cells from healthy cells, which are attractive targets for adoptive cell therapies. However, the process of precisely identifying the neoepitopes to target is complex and challenging. One method to identify such neoepitopes is Mass Spectrometry (MS) when used in conjunction with elution of peptides bound to a specific Human Leukocyte Antigen (HLA) allele.

Scientists at NIAID have developed two immortalized stable B cell lines from rhesus macaques that can have value as research tools for the discovery of neutralizing antibodies of simian origin against HIV and that may have value in the development of an HIV vaccine. These B cell lines encode human Bcl-6 and Bcl-xL proteins, which are major regulators of apoptosis. These B cell lines are derived from the lymph node of a rhesus macaque (RM) that was infected with SHIV.CH505.

       Emergence of highly transmissible SARS-CoV-2 variants of concern that are resistant to current therapeutic antibodies highlights the need for continuing discovery of broadly reactive antibodies.

There are five known Ebolavirus species: Ebola virus (Zaire ebolavirus); Sudan virus (Sudan ebolavirus or SUDV); Taï Forest virus (Taï Forest ebolavirus, formerly Cote d'Ivoire ebolavirus); Bundibugyo virus (Bundibugyo ebolavirus); and Reston virus (Reston ebolavirus). Last year an ebolavirus outbreak resulted in 164 cases and 55 deaths. While there is an FDA-approved Ebola virus vaccine authorized for use against Ebola virus infections, ERVEBO, this vaccine is not effective against SUDV due to the significant variation between Ebola virus and SUDV.