Immune status following alemtuzumab treatment in human CD52 transgenic mice

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Immune status following alemtuzumab treatment in human CD52 transgenic mice

Alemtuzumab is a monoclonal antibody against the CD52 antigen present at high levels on the surface of lymphocytes. While treatment of multiple sclerosis patients with alemtuzumab results in marked depletion of lymphocytes from the circulation, it has not been associated with a high incidence of serious infections. In a human CD52 transgenic mouse, alemtuzumab treatment showed minimal impact on...

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CD52-Negative NK Cells Are Abundant in the Liver and Less Susceptible to Alemtuzumab Treatment

BACKGROUND T-cell depleting strategies have become an integral part of immunosuppressive regimens in organ transplantation. Alemtuzumab is a humanized monoclonal antibody against CD52, a cell-surface antigen on several immune cells. It has been suggested that lymphocyte depletion increases the risk of serious infections. However, this has not been observed with short-term alemtuzumab treatment ...

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Peripheral blood but not tissue dendritic cells express CD52 and are depleted by treatment with alemtuzumab.

CAMPATH antibodies recognize CD52, a phosphatidylinositol-linked membrane protein expressed by mature lymphocytes and monocytes. Since some antigen-presenting dendritic cells (DCs) differentiate from a monocytic progenitor, we investigated the expression of CD52 on dendritic cell subsets. Four-color staining for lineage markers (CD3, 14, 16, 19, 20, 34, and 56), HLA-DR, CD52, and CD123 or CD11c...

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Human-like immune responses in CD46 transgenic mice.

Neisseria meningitidis is a major cause of sepsis and/or meningitis. These bacteria normally cause disease only in humans, however, mice expressing human CD46 are susceptible to meningococcal disease. To explain the sensitivity of CD46 transgenic mice to meningococci, we evaluated early immune responses. Stimulation of TNF, IL-6, and IL-10 was stronger in CD46 transgenic mice compared with nont...

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ژورنال

عنوان ژورنال: Journal of Neuroimmunology

سال: 2013

ISSN: 0165-5728

DOI: 10.1016/j.jneuroim.2013.04.018