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Circulation. 2005;112:1918-1920
doi: 10.1161/CIRCULATIONAHA.105.571943
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(Circulation. 2005;112:1918-1920.)
© 2005 American Heart Association, Inc.


Editorial

Gaining More From Gamma Globulins

Karen Y. Stokes, PhD; D. Neil Granger, PhD

From the Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, La.

Correspondence to D. Neil Granger, PhD, Dept of Molecular and Cellular Physiology, LSU Health Sciences Center, 1501 E Kings Hwy, Shreveport, LA 71130-3932. E-mail dgrang@lsuhsc.edu


Key Words: Editorials • endothelium • ischemia • cell adhesion molecules • leukocytes


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The use of intravenous immunoglobulin (IVIg), which is immunoglobulin G pooled from thousands of healthy donors, in the treatment of immunodeficient and autoimmune diseases has grown during the past 2 decades. Although its initial application was largely limited to replacement therapy in hypogammaglobulinemia, IVIg is gaining acceptance as therapy for autoimmune thrombocytopenia purpura, and a number of other autoimmune diseases such as multiple sclerosis.1 Although the exact mechanisms underlying the protection conferred by IVIg in these immune disorders remain undefined, several potential molecular and cellular targets have been proposed. For example, IVIg can block Fc receptors on macrophages and effector cells to reduce the phagocytic capacity of these cells. IVIg may also regulate the immune response by reacting with a number of membrane receptors on T cells, B cells, and monocytes that are pertinent to autoreactivity and induction of tolerance to self.1 Recent work has also revealed a beneficial effect of IVIg in systemic inflammatory disorders such as sepsis and asthma. It has been suggested that IVIg may exert its antiinflammatory effects by attenuating complement-mediated attack,2 inducing antiinflammatory cytokines, and reducing the production of proinflammatory cytokines such as tumor necrosis factor-{alpha}, interferon-{gamma} and interleukin-13 (Figure). Many of these mechanistic studies of IVIg effects on the inflammatory response are based on in vitro models and in vivo data are lacking.


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Differential effects of IVIg on several steps in the inflammatory cascade: Numbers denote potential antiinflammatory actions of IVIg; letters denote possible adverse effects of IVIg that may worsen . . . [Full Text of this Article]


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Targeting Adhesion Molecules as a Potential Mechanism of Action for Intravenous Immunoglobulin
Varinder Gill, Christopher Doig, Derrice Knight, Emma Love, and Paul Kubes
Circulation 2005 112: 2031-2039. [Abstract] [Full Text]