The In Vivo Cytokine Capture Assay for Measurement of Cytokine Production in the Mouse

Finkelman, Fred D.; Morris, Suzanne C.; Orekhova, Tatyana; Sehy, David

doi:10.1002/0471142735.im0628s54

Cited by 38 publications

(44 citation statements)

References 19 publications

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“…IL-6 serum levels were measured by an in vivo cytokine capture assay as described (51). IL-33 in cell-culture supernatants was detected and measured by ELISA as suggested by the manufacturer (eBioscience).…”

Section: Methodsmentioning

confidence: 99%

Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs

Fiebiger

Maamary

Pincetic

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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The antiinflammatory activity of intravenous immunoglobulin (IVIG) is dependent on the presence of sialic acid in the core IgG fragment crystallizable domain (Fc) glycan, resulting in increased conformational flexibility of the C H 2 domain with corresponding modulation of Fc receptor (FcR) binding specificity from type I to type II receptors. Sialylated IgG Fc (sFc) increases the activation threshold of innate effector cells to immune complexes by stimulating the upregulation of the inhibitory receptor FcγRIIB. We have found that the structural alterations induced by sialylation can be mimicked by specific amino acid modifications to the C H 2 domain. An IgG Fc variant with a point mutation at position 241 (F→A) exhibits antiinflammatory activity even in the absence of sialylation. F241A and sFc protect mice from arthritis in the K/BxN-induced model and, in the T cell-mediated experimental autoimmune encephalomyelitis (EAE) mouse model, suppress disease by specifically activating regulatory T cells (T reg cells). Protection by these antiinflammatory Fcs in both antibody-and T cell-mediated autoimmune diseases required type II FcRs and the induction of IL-33. These results further clarify the mechanism of action of IVIG in both antibody-and T cellmediated inflammatory diseases and demonstrate that Fc variants that mimic the structural alterations induced by sialylation, such as F241A, can be promising therapeutic candidates for the treatment of various autoimmune disorders.IgG Fc sialylation | conformational change | antiinflammatory | T reg cells

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Section: Methodsmentioning

confidence: 99%

Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs

Fiebiger

Maamary

Pincetic

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…In vivo IL-4 secretion was measured by IVCCA (40,41). Mice were injected with biotinylated anti-IL-4 mAb (BVD4-1D11) (42) at the time of trinitrophenyl ovalbumin (TNP-OVA) challenge.…”

Section: Methodsmentioning

confidence: 99%

Identification of markers that distinguish IgE- from IgG-mediated anaphylaxis

Khodoun

Strait

Armstrong

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

124

107

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IgG-mediated anaphylaxis occurs in mice and may contribute to human reactions to infused drugs. To distinguish IgE- from putative IgG-mediated human anaphylaxis, we developed blood markers for murine anaphylaxis and evaluated their human relevance. Both IgG- and IgE-mediated anaphylaxis were characterized by decreased basophil and monocyte percentages and an increased neutrophil percentage in mouse blood. IgE- but not IgG-mediated murine anaphylaxis was accompanied by large increases in IL-4 secretion, plasma soluble IL-4 receptor-α (IL-4Rα) concentration, and T-cell membrane IL-4Rα expression. T-cell IL-4Rα expression also increased when mice that express human Fcε receptor Iα were sensitized with IgG-depleted serum from a peanut-allergic individual and challenged with peanut extract. Increased T-cell IL-4Rα expression is likely to also be a marker for human IgE-mediated anaphylaxis, because IgE-activated human basophils secrete IL-4, and IL-4 increases human T-cell IL-4Rα expression in vitro. Murine IgG- but not IgE-mediated anaphylaxis was characterized by decreased neutrophil Fcγ receptor III (FcγRIII) expression that was observed even when the antigen dose was insufficient to induce shock. Human neutrophils cultured with IgG immune complexes also lost FcγRIII. These observations suggest that decreased blood neutrophil FcγRIII expression without increased IL-4Rα expression can be used to determine whether and when IgG-mediated anaphylaxis occurs in man.

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“…The IVCCA (32,33) was used to measure in vivo production of IL-2, IL-4, IL-6, IL-10, IFN-␥, and TNF. Briefly, mice were injected i.v.…”

Section: Ivccamentioning

confidence: 99%

Diesel Exhaust Particles Suppress In Vivo IFN-γ Production by Inhibiting Cytokine Effects on NK and NKT Cells

Finkelman

Yang

Orekhova

et al. 2004

The Journal of Immunology

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Diesel exhaust particles (DEP) have strong, selective Th2 adjuvant activity when inhaled with conventional Ags. We used a novel technique for measuring in vivo cytokine production to investigate possible mechanisms by which DEP might promote a Th2 response. Injection of DEP i.p. stimulated IL-6 secretion, but failed to increase IL-4, IL-10, or TNF-α secretion, and decreased basal levels of IFN-γ. When injected with or before LPS, DEP had little effect on the LPS-induced TNF-α responses, but partially inhibited the LPS-induced IL-10 response and strongly inhibited the LPS-induced IFN-γ response. DEP also inhibited the IFN-γ responses to IL-12, IL-12 plus IL-18, IL-2, and poly(I · C). DEP treatment had little effect on the percentages of NK and NKT cells in the spleen, but inhibited LPS-induced IFN-γ production by splenic NK and NKT cells. In contrast, DEP failed to inhibit the IFN-γ response by anti-CD3 mAb-activated NKT cells. Taken together, these observations suggest that DEP inhibit Toll-like receptor ligand-induced IFN-γ responses by interfering with cytokine signaling pathways that stimulate NK and NKT cells to produce IFN-γ. Our observations also suggest that DEP may promote a Th2 response by stimulating production of inflammatory cytokines while simultaneously inhibiting production of IFN-γ, and raise the possibility that the same mechanisms contribute to the association between DEP exposure and asthma.

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The In Vivo Cytokine Capture Assay for Measurement of Cytokine Production in the Mouse

Cited by 38 publications

References 19 publications

Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs

Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs

Identification of markers that distinguish IgE- from IgG-mediated anaphylaxis

Diesel Exhaust Particles Suppress In Vivo IFN-γ Production by Inhibiting Cytokine Effects on NK and NKT Cells

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