BOSTON, Nov. 8 /PRNewswire/ -- MedImmune, Inc. today announced it will present 11 abstracts at the 71st Annual Meeting of the American College of Rheumatology, demonstrating the company's breadth of ongoing, multi-stage research evaluating the origins and effects of inflammatory disease and novel disease pathways.

"MedImmune is pleased to present data that may provide significant insights into the nature of systemic autoimmune diseases as well as potential new treatment options for patients in need," said Barbara White, M.D., vice president, clinical development, inflammatory disease.

Investigators will present results from eight studies in systemic lupus erythematosus (SLE), one in scleroderma, one in rheumatoid arthritis and one evaluating therapeutic B-cell depletion across multiple autoimmune diseases.

"The research presented at ACR exemplifies MedImmune's pioneering role in identifying new pathways involved in rheumatic disease and developing targeted monoclonal antibodies (MAbs) as potential treatments," said Anthony Coyle, Ph.D., vice president, respiratory, inflammation and autoimmune disease research.

MedImmune research scheduled to be presented includes: -- MEDI-545, an Anti-Interferon Alpha Monoclonal Antibody, Shows Evidence of Clinical Activity in Systemic Lupus Erythematosus (Presentation #1315, ACR Concurrent Abstract Session #025-1, SLE: Novel Therapies) - Daniel J. Wallace, M.D., Friday, November 9, 2007 from 2:30 - 2:45 p.m. -- Safety of MEDI-545, an Anti-Interferon-. Monoclonal Antibody, in MI- CP126, a Phase I Trial in Systemic Lupus Erythematosus (SLE) (Presentation/Poster Board #428, Poster Session #125-01, SLE: Clinical Aspects and Treatment I) - Joan T. Merrill, M.D., Thursday, November 8, 2007 from 9:00 - 11:00 a.m. -- Identification of Novel Autoantibodies in Sera from SLE Patients Using High Density Auto-Antigen Arrays: Relationship to Type I Interferon Gene Signature and Bioactivity (Presentation #761, Session #3212, REF Edmund L. Dubois, M.D., Memorial Lectureship) -Jonathan Zmuda, M.D., Thursday, November 8, 2007 from 4:30 - 6:00 p.m. -- Antagonizing HMBG1 Blocks Inflammation and Tissue Damage in Experimental Arthritis (Presentation #2135, ACR Concurrent Abstract Session #001-2, Novel Molecular Mediators and Treatments) - Su-Yau Mao, M.D., Saturday, November 10, 2007 from 5:15 - 5:30 p.m. -- Antagonizing Type-I Interferon Receptor Ameliorates Lupus Disease in Autoimmune NZB/W F1 Mice (Presentation/Poster Board #2134, Poster Session #001-2, Novel Molecular Mediators and Treatments) - Yan Xu, M.D., Saturday, November 10, 2007 from 5:00 - 5:15 p.m. -- Neutralization of Type I IFN Inducible Genes in Phase I Trial of Anti- IFN alpha mAb for the Treatment of SLE: Utility as Pharmacodynamic Markers (Presentation/Poster Board #429, Poster Session #125-01, SLE: Clinical Aspects and Treatments I) - Yihong Yao, M.D., Thursday, November 8, 2007 from 9:00 - 11:00 a.m. -- Anti-IFN-alpha Antibody Neutralization of Early and Late Transcriptional Responses in PBMC Stimulated with Serum from SLE Patients (Presentation #840, Poster Board #72, Poster Session #133-02, Genetics, Genomics and Proteomics II) - Wendy L. Trigona, M.D., Friday, November 9, 2007 from 9:00 - 11:00 a.m. -- Direct Quantitation of Interferon-Related Transcripts in Whole Blood of SLE Patients Without RNA Isolation and Reverse Transcriptase Real-Time PCR Using Panomics QuantiGene(R)Plex Technology: Applications in a Phase I Clinical Trial (Presentation/Poster Board #430, Poster Session #25-01, Clinical Aspects and Treatment I) - Jonathan Zmuda, M.D., Thursday, November 8, 2007 from 9:00 - 11:00 a.m. -- Antagonizing RAGE Inhibits Immune Complex Induced IFN alpha Gene Signature In Human PBMC (Presentation/Poster Board #132, Poster Session #101-01, Cytokines, Mediators and Gene Regulation I) - Bo Chen, M.D., Thursday, November 8, 2007 from 9:00 - 11:00 a.m. -- Generation of a Humanized Anti-CD19 Antibody with Superior Effector Function by Combining Fab and Fc Modifications (Presentation #1417, Poster Board #31, Poster Session #104-01, B-Cell Biology and Targets in Autoimmune Disease) - Ronald Herbst, M.D., Saturday, November 10, 2007 from 9:00 - 11:00 a.m. -- Role of Type I Interferons in a Murine Model of Scleroderma (Presentation/Poster Board #46, Poster Session #122-01, Systemic Sclerosis, Fibrosing Syndromes and Raynaud's: Pathogenesis, Animal Models and Genetics) - Tracey A. Delaney, M.D., Thursday, November 8, 2007 from 9:00 - 11:00 a.m.

About MEDI-545

MEDI-545 is a fully human MAb targeting interferon-alpha. Published data indicate that levels of interferon-alpha are elevated in many patients with active SLE and other autoimmune disorders, and may be associated with disease activity. Preclinical data from animal models suggest that MEDI-545 may suppress the abnormal immune activity associated with lupus by binding to multiple interferon-alpha subtypes seen in the serum of lupus patients. MedImmune and Medarex, Inc. entered a collaboration to develop antibodies targeting interferon-alpha in 2004.

About HMGB1 (High Mobility Group Box Chromosomal Protein 1)

HMGB1, a pro-inflammatory protein secreted by different cell types, is part of the body's response to trauma and infection. HMGB1 is expressed at high levels beginning 12 to 72 hours after an injury, which is about the time inflammation-associated tissue damage begins. Because of the timing and duration of expression of HMGB1, it may be an important factor in the sequence of events that result in severe tissue damage following injury or during chronic inflammation. MedImmune's HMGB1 program is being conducted in collaboration with Critical Therapeutics, Inc.

About Anti-CD19

CD19 is a B-cell lineage-specific molecule involved in immune regulation. Preclinical studies indicate that antibodies targeting this antigen may block B-cell activity that is associated with many tumors and autoimmune diseases, including multiple myeloma, B-cell lymphomas, rheumatoid arthritis and lupus. Early research on the potential therapeutic benefits of blocking this molecule has been conducted by Thomas F. Tedder, Ph.D., chairman of the Department of Immunology at Duke University Medical Center and leading authority in B-cell biology.

About Lupus

Approximately 350,000 individuals in the United States are affected with lupus, a chronic inflammatory disease that causes the body to attack its own tissues and organs, including the skin, joints, blood and kidneys. Treatments for lupus include anti-inflammatory drugs, antimalarials, corticosteroids and drugs approved for other purposes, such as immunosuppressive agents given to cancer patients undergoing chemotherapy or medicines developed to treat arthritis patients. Lupus occurs about 10 times more frequently in adult females than adult males, and is two to three times more common among African Americans, Hispanics, Asians and Native Americans.

About Scleroderma

Scleroderma is a chronic, autoimmune disease in which normal tissue is replaced with dense, thick fibrous tissue. In patients with scleroderma, the immune system triggers other cells to produce collagen in excess quantities. This excess collagen is deposited in the skin and organs, which causes hardening and thickening (similar to the scarring process). Although it most often affects the skin, scleroderma can also affect the gastrointestinal tract, lungs, kidneys, heart, blood vessels, muscles and joints. Scleroderma, in its most severe forms, may be life-threatening.

About MedImmune

MedImmune strives to provide better medicines to patients, new medical options for physicians and rewarding careers to employees. With approximately 3,000 employees worldwide and headquarters in Maryland, MedImmune is dedicated to advancing science and medicine to help people live better lives and is wholly owned by AstraZeneca plc . For more information, visit MedImmune's website at http://www.medimmune.com.