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Sjögren's syndrome is an autoimmune disease that attacks salivary glands resulting in chronic dry mouth and dry eyes. Currently, there is no single diagnostic test to confirm the presence of Sjögren's. Physicians presently reach diagnosis after conducting a series of blood and functional tests for tear and salivary production. Diagnosis is further complicated as Sjögren's symptoms frequently mimic those of other autoimmune diseases (e.g., lupus, rheumatoid arthritis, etc.) and is often overlooked as dryness associated with medications being taken by the patient.

The subject technology discloses a tissue engineering method for treating cartilage damage. Stem cells from bone marrow are attached to a novel scaffold, hyaluronic acid-coated fibrin microbeads, and transferred to a live host to form cartilage. The regenerated cartilage is stable and not hypertrophic, which has been problematic in the current regenerative methods.

Autoimmune inflammatory diseases occur in greater than five percent of the United States population; this disease group includes asthma, multiple sclerosis, rheumatoid arthritis, and lupus. Treatments generally include immunosuppressants or anti-inflammatory drugs, which can have serious side effects; recently, more specific immunomodulatory therapies such as TNF-alpha antagonists have been developed.

Systemic lupus erythematosus (SLE) is a multi-organ inflammatory disease characterized by a significant morbidity and mortality related to both disease evolution as well as therapeutic side effects. At least half of SLE patients develop lupus nephritis.

The invention relates to recombinant chimeric rabbit/human monoclonal antibody fragments (Fabs) against hepatitis B Virus e-antigen (HBeAg), notably Fab me6. Viral hepatitis is the seventh leading cause of death worldwide. Hepatitis B core antigen (HBcAg) forms an icosahedral structure containing the viral genome. Both the HBcAg and the HBeAg of interest here are expressed by two different start codons of the viral C gene. Unlike the related HBcAg which activates type 1 T helper (Th1) cells leading to immune attack, the HBeAg activates Th2 cells which promote immune tolerance.

The present invention provides a therapeutic method for the treatment of autoimmune or autoinflammatory diseases by first breaking down the dysregulated immune system and then reprogramming the immune system to restore tolerance to the patient's self-antigens by induction of antigen specific regulatory T cells. The inventors have shown that only with the combination of apoptosis, phagocytes, and antigen can antigen-specific regulatory T cells (T_reg) cells be optimally generated to develop long-term immune tolerance.

Rapid point-of-care, antibody-based testing is not available for the diagnosis of autoimmune and most infectious diseases. For detecting autoantibodies associated with most autoimmune conditions, fluid-phase immunoprecipitation assays are required. However, these assays usually involve radioactivity and are not feasible for point-of-care applications. The subject invention describes methods of using neodymium magnet for diagnosis of infectious and autoimmune diseases including lupus, Sjögren's syndrome, type I diabetes, HIV and Lyme disease.

This technology includes antibodies to apolipoprotein L1 (ApoL 1) to be used in basic science laboratory studies. ApoL 1 is a protein that is present within cells and circulates as component of high-density lipoprotein. Its functions are not well understood. Recently APOL 1 genetic variants have been shown to be highly associated with kidney disease in African Americans.

Novel A₃ adenosine antagonists available for licensing. A₃ receptors are particularly highly expressed in inflammatory cells, making it a potentially desirable target for inflammatory diseases. This technology relates to highly specific antagonists and partial agonists of A₃ adenosine receptors, which are negatively coupled to adenylate cyclase and have been broadly implicated in inflammation, cardiovascular disease, endocrine conditions and cancer. Further, A₃ adenosine receptors have been implicated in asthma and glaucoma.