Intravenous immunoglobulin induces interferon-? and interleukin-6in vivo

Ling, Zaodung; Yeoh, Eunice; Webb, B.; Farrell, Kevin; Doucette, Jocelyne; Matheson, David S.

doi:10.1007/bf00920238

Cited by 59 publications

(32 citation statements)

References 19 publications

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“…However, several proinflammatory cytokines were found to be increased in patients treated with high doses of IVIg (Ling et al, 1993;Aukrust et al, 1994;Ibanez et al, 2005) or in anti-D-treated ITP patients (Semple et al, 2002;Cooper et al, 2004), in addition to the anti-inflammatory cytokines discussed above. The presence of pro-inflammatory cytokines could thus interfere with the expected beneficial effects of anti-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Absence of cytokine modulation following therapeutic infusion of intravenous immunoglobulin or anti‐red blood cell antibodies in a mouse model of immune thrombocytopenic purpura

2007

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SummaryHuman intravenous immunoglobulin (IVIg) and anti‐D immunoglobulin preparations are used in the treatment of immune thrombocytopenic purpura (ITP). One mechanism proposed to explain their therapeutic effects in ITP patients is the induction of expression of anti‐inflammatory cytokines, such as interleukin (IL)‐10 or IL‐1ra, leading to a reduction of phagocytic activity of the reticuloendothelial system. However, increased expression of pro‐inflammatory cytokines was also noted following treatment of ITP patients, raising doubt on the actual contribution of anti‐inflammatory cytokines in the therapeutic effects of IVIg and anti‐D immunoglobulins. The present study evaluated the in vivo modulation of expression of a large array of inflammatory cytokines using a mouse model of thrombocytopenia. IVIg was not found to modulate cytokine expression although it efficiently prevented thrombocytopenia. In contrast, protective (M1/69) and non‐protective (TER‐119) anti‐mouse red blood cell (RBC) antibodies (mimicking anti‐D treatment) both increased the expression of CXCL‐1 and CXCL‐5. Thus, there was no relationship between inflammatory cytokine expression and prevention of thrombocytopenia by IVIg or anti‐mouse RBC in the ITP mouse model. These results suggest that the increase in cytokine expression observed in ITP patients following IVIg or anti‐D infusion is not required for their therapeutic effects but may rather represent a side‐effect of the treatment.

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Section: Discussionmentioning

confidence: 99%

Absence of cytokine modulation following therapeutic infusion of intravenous immunoglobulin or anti‐red blood cell antibodies in a mouse model of immune thrombocytopenic purpura

2007

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“…Cell suspensions (2 Â 10 6 /ml) were incubated at 37 C in a 5% CO 2 humidified air atmosphere for up to 24 h. Samples treated only with CCM were used as control. [19].…”

Section: Methodsmentioning

confidence: 99%

Interaction of Human Immunoglobulin G with CD16 on Natural Killer Cells: Ligand Clearance, FcγRIIIA Turnover and Effects of Metalloproteinases on FcγRIIIA‐Mediated Binding, Signal Transduction and Killing‡

Moţa¹,

Moldovan²,

Călugăru³

et al. 2004

Scand J Immunol

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Human natural killer (NK) cells express low-affinity Fc immunoglobulin G (IgG) receptor (FcgRIIIA/CD16). The binding of monomeric IgG (mIgG) and F(ab 0 ) 2 fragments of 3G8 anti-CD16 monoclonal antibody (mAb) to FcgRIIIA was investigated by flow cytometry. Over 90% of NK cells bound endogenous IgG, and during incubation at 37 C, the FcgRIIIA occupancy decreased slowly. Approximately 90% of NK cells bind mIgG or F(ab 0 ) 2 fragments of 3G8 anti-CD16 mAb. The calculated half-time (T 1/2 ) of in vitro mIgG dissociation from FcgRIIIA was 130 min. By cross-linking the mIgG ligand with F(ab 0 ) 2 fragments of anti-human IgG antibody, the T 1/2 decreases to 85 min. In kinetics study, it has been shown that 125 I-mIgG bound to FcgRIIIA is slowly released in the culture supernatant, maybe eluted at acid pH, or partially internalized and degraded. The binding of IgG to FcgRIIIA was increased by 53.8% on cells cultured in the presence of RU36156, a matrix metalloproteinase (MMP) inhibitor. Furthermore, an increase in phosphorylation of Lyn tyrosine kinase, after cross-linking of mIgG-FcgRIIIA complex, was observed on NK cells treated with RU36156. When the FcgRIIIA was occupied by mIgG, the capacity of NK cells to kill K562 target cells was decreased by RU36156, because the MMP inhibitor protects CD16 from proteolysis. Our data demonstrate that binding of mIgG to human NK cells is followed by ligand dissociation and/or internalization, enzymatic degradation and exocytosis. The RU36156 MMP inhibitor protects FcgRIIIA from cleavage, augments NK-cell activation and may interfere in their killing capacity.

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“…Clinical studies in humans have found modest cytokine changes to occur within hours to days after i.v. IgG infusion but have used doses an order of magnitude higher (400 to 600 mg/kg) than those administered here (29). In a study of HIV-infected individuals, TNF-␣ levels were found to decline by 5 days after i.v.…”

Section: Figmentioning

confidence: 99%

Magnitude and Quality of Cytokine and Chemokine Storm during Acute Infection Distinguish Nonprogressive and Progressive Simian Immunodeficiency Virus Infections of Nonhuman Primates

Keating

Heitman

et al. 2016

J Virol

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Acute human immunodeficiency virus (HIV) infection represents a period of intense immune perturbation and activation of the host immune system. Study of the eclipse and viral expansion phases of infection is difficult in humans, but studies in nonpro- IMPORTANCENHP models of HIV infection constitute a powerful tool with which to study viral pathogenesis in order to gain critical information for a better understanding of HIV infection in humans. Here we studied progressive and nonprogressive simian immunodeficiency virus (SIV) infection models in both natural and nonnatural host NHP species. Regardless of the pathogenicity of the virus infection and regardless of the NHP species studied, the magnitude of viremia, as measured by area under the curve, during the first 4 weeks of infection correlated positively with viremia in chronic infection. The magnitude of cytokine and chemokine responses during primary infection also correlated positively with both acute-phase and chronic viremia. However, the pattern and levels of specific cytokines and chemokines produced differed between nonprogressive and progressive SIV infection models. The qualitative differences in the early immune response in pathogenic and nonpathogenic infections identified here may be important determinants of the subsequent disease course.

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Intravenous immunoglobulin induces interferon-? and interleukin-6in vivo

Cited by 59 publications

References 19 publications

Absence of cytokine modulation following therapeutic infusion of intravenous immunoglobulin or anti‐red blood cell antibodies in a mouse model of immune thrombocytopenic purpura

Absence of cytokine modulation following therapeutic infusion of intravenous immunoglobulin or anti‐red blood cell antibodies in a mouse model of immune thrombocytopenic purpura

Interaction of Human Immunoglobulin G with CD16 on Natural Killer Cells: Ligand Clearance, FcγRIIIA Turnover and Effects of Metalloproteinases on FcγRIIIA‐Mediated Binding, Signal Transduction and Killing‡

Magnitude and Quality of Cytokine and Chemokine Storm during Acute Infection Distinguish Nonprogressive and Progressive Simian Immunodeficiency Virus Infections of Nonhuman Primates

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