Effects of Intravenous Immunoglobulins (IVIG) on Peripheral Blood B, NK, and T Cell Subpopulations in Women with Recurrent Spontaneous Abortions: Specific Effects on LFA-1 and CD56 Molecules

Effect of high-dose intravenous immunoglobulin on serum chemistry, hematology, and lymphocyte subpopulations: Assessments based on controlled treatment trials in patients with neurological diseases

“…7,11,25,33,34 In spite of the significant induction of neutropenia, no bacterial infections were observed. Among erythropoeitic cells, the observed reduction in the platelet count (Table 2) was a surprise, considering the beneficial effect of IVIG therapy in idiopathic thrombocytopenic purpura.…”

Targeting Adhesion Molecules as a Potential Mechanism of Action for Intravenous Immunoglobulin

“…25 There is also indirect evidence that IVIg could reduce the expression of lymphocyte function-associated antigen-1 (LFA-1) on neutrophils, thereby reducing leukocyte adhesion. 26 In vivo studies using intravital microscopy have demonstrated that IVIg could reduce leukocyte recruitment into the liver after systemic administration of tumor necrosis factor-␣ or lipopolysaccharide. 27 However, those authors proposed a mechanism that involved macrophage activity.…”

Association of Selected Phenotypic Markers of Lymphocyte Activation and Differentiation with Perinatal Human Immunodeficiency Virus Transmission and Infant Infection

“…Likewise, use of prenatal IVIG in other disorders is not associated with lymphocyte activation or premature maturation of the neonatal immune system (26). While specific immunological effects of HIVIG in pregnancy have not been studied, IVIG treatment in pregnancy does not appear to affect levels of CD3ϩCD8 ϩ or CD3 ϩ lymphocytes (17,30), but does reduce peripheral blood NK cells (15). IVIG appears to exert its therapeutic effects in autoimmune and alloimmune disorders by down-regulation of costimulatory molecules associated with modulation of cytokine secretion, with resultant inhibition of autoreactive and alloreactive T-cell activation and proliferation (2); by reduction of intact B cell and monocyte cell numbers, modulation of surface molecule expression on B cells, and deletion of B and T cells by apoptosis with resultant inhibition of optimal T-cell activation (34); and by inhibition of cytokine-induced NF-B activation and blocking of Fc␥RIII on cell membranes (11,12).…”