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Gamma Globulin (gamma + globulin)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Rapid clinical and CSF response to intravenous gamma globulin in acute disseminated encephalomyelitis

EUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2001
S. J. Pittock
[source]

Increased levels of Monocyte Chemoattractant Protein-1 in cerebrospinal fluid with gamma globulin induced meningitis

ACTA PAEDIATRICA, Issue 2 2010
Takeshi Asano
No abstract is available for this article. [source]

Immune complex-stimulated production of interleukin-12 in peripheral blood mononuclear cells is regulated by the complement system

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2004
A. TEJDE
SUMMARY Immune complexes (IC) can induce cytokine production in vitro. While immune aggregates (IA) consisting of heat-aggregated gamma globulin (HAGG) as model IC increased interleukin (IL)-10 levels in cell cultures with native human serum, IL-12p40/p70 production was inhibited. Three series of experiments suggested that the effects of IA on IL-12 production depended on a functionally intact complement system: (1) heat-inactivation of serum inverted the inhibitory effect of IA on IL-12p40/p70 production; (2) IA-induced IL-12p40 production in a C4 deficient serum was lowered by addition of C4; and (3) addition of the peptide compstatin, which blocks C3 activation, mimicked the effects of heat inactivation on IL-12p40 levels. Neutralization of IL-12 resulted in modestly increased IL-10 levels, while neutralization of IL-10 had no effects on IL-12p40 production. IA-induced production of IL-10 was partially blocked by anti-Fc,,RII antibodies, whereas Fc,,R or CR blockade had no effect on IL-12p40 production. IC and local or systemic complement activation characterize rheumatoid arthritis, systemic lupus erythematosus and many malignancies. Different and complement-dependent effects on the production of IL-10 and IL-12 can be of importance in these diseases, where control of the complement system might be a way to direct IC-induced cytokine production in either a type 1 or type 2 direction. [source]

Increased expression of Fc, receptors II and III on macrophages of rheumatoid arthritis patients results in higher production of tumor necrosis factor , and matrix metalloproteinase

ARTHRITIS & RHEUMATISM, Issue 4 2003
Arjen B. Blom
Objective To evaluate Fc, receptor (Fc,R) expression on synovial macrophages from rheumatoid arthritis (RA) patients and to determine whether this expression correlates with the production of the proinflammatory cytokines tumor necrosis factor , (TNF,), interleukin-1, (IL-1,), IL-12, and matrix metalloproteinase 1 (MMP-1). We also sought to determine whether mature macrophages from RA patients express aberrant levels of Fc,RI, Fc,RII, and Fc,RIII, and to determine the production of inflammatory mediators after immune complex (IC) stimulation. Methods Immunohistochemistry was performed on cryostat sections of synovial biopsy specimens obtained from 27 RA patients and 5 controls. Fc,R I, II, and III were detected, as well as the proinflammatory mediators IL-1, TNF,, IL-12, and MMP-1. Monocytes were isolated from the blood of 10 RA patients and 10 healthy controls and cultured for 7 days with macrophage colony-stimulating factor to obtain macrophages. Using fluorescence-activated cell sorting, the expression of Fc,RI, Fc,RII, and Fc,RIII was determined. On day 7, macrophages were stimulated with heat-aggregated gamma globulins (HAGGs) for 24 hours. Production of cytokines was measured using enzyme-linked immunosorbent assay, and production of gelatinases/collagenases was measured by degradation of fluorescent gelatin. Results Immunohistochemistry showed higher Fc,RII and Fc,RIII expression in RA synovium than in controls. Fc,RII and Fc,RIII, but not Fc,RI, were highly correlated with the number of synovial macrophages. Consistent with this, TNF, expression correlated positively with Fc,RIII expression. Moreover, MMP-1 expression strongly correlated with Fc,R I, II, and III expression. Mature macrophages from RA patients showed significantly enhanced expression of Fc,RII and Fc,RIII compared with controls. Twenty-four hours after stimulation of RA macrophages with HAGGs, significantly higher production of TNF, and gelatinase/collagenase was measured. Conclusion RA synovium and mature RA macrophages express significantly elevated levels of Fc,RII and Fc,RIII, resulting in much higher production of TNF, and gelatinase/collagenase after IC stimulation. These data suggest that disturbed expression of Fc,R on mature synovial macrophages is involved in the pathology of RA. [source]