Intravenous immunoglobulin-mediated expansion of regulatory T cells in autoimmune patients is associated with increased prostaglandin E2 levels in the circulation

Maddur, Mohan S.; Trinath, Jamma; Rabin, Magalie; Bolgert, Françis; Guy, Moneger; Vallat, Jean‐Michel; Magy, Laurent; Balaji, Kithiganahalli Narayanaswamy; Kaveri, Srini V.; Bayry, Jagadeesh

doi:10.1038/cmi.2014.117

Cited by 35 publications

(27 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In terms of their roles in immune function, PGE 2 has been shown to have both pro- [31] and anti-inflammatory [32] properties, complicating interpretation of its increase in those with BMIs>35. However, it is generally thought of as an inhibitor of both innate and adaptive immunity, in part by increasing myeloid derived suppressor cells (MDSCs) [32] and Tregs [33]. An increase might thus hinder the elimination of cancer cells but might be helpful in preventing autoimmune disorders.…”

Section: Fig 6 Obesity Increases Cd4+ T Cells and Tregs And Reduces mentioning

confidence: 99%

Exploratory examination of inflammation state, immune response and blood cell composition in a human obese cohort to identify potential markers predicting cancer risk

et al. 2020

View full text Add to dashboard Cite

Obesity has reached epidemic proportions and is often accompanied by elevated levels of pro-inflammatory cytokines that promote many chronic diseases, including cancer. However, not all obese people develop these diseases and it would be very helpful to identify those at high risk early on so that preventative measures can be instituted. We performed an extensive evaluation of the effects of obesity on inflammatory markers, on innate and adaptive immune responses, and on blood cell composition to identify markers that might be useful in distinguishing those at elevated risk of cancer. Plasma samples from 42 volunteers with a BMI>35 had significantly higher CRP, PGE 2 , IL-1RA, IL-6 and IL-17 levels than 34 volunteers with normal BMIs. Of the cytokines and chemokines tested, only IL-17 was significantly higher in men with a BMI>35 than women with a BMI>35. As well, only IL-17 was significantly higher in those with a BMI>35 that had type 2 diabetes versus those without type 2 diabetes. Whole blood samples from participants with a BMI>35, when challenged with E. coli, produced significantly higher levels of IL-1RA while HSV-1 challenge resulted in significantly elevated IL-1RA and VEGF, and a non-significant increase in G-CSF and IL-8 levels. T cell activation of PBMCs, via anti-CD3 plus anti-CD28, resulted in significantly higher IFNγ production from volunteers with a BMI>35. In terms of blood cells, red blood cell distribution width (RDW), monocytes, granulocytes, CD4 + T cells and Tregs were all significantly higher while, natural killer (NK) and CD8 + T cells were all significantly lower in the BMI>35 cohort, suggesting that obesity may reduce the ability to kill nascent tumor cells. Importantly, however, there was considerable person-to-person variation amongst participants with a BMI>35, with some volunteers showing markedly different values from controls and others

show abstract

Section: Fig 6 Obesity Increases Cd4+ T Cells and Tregs And Reduces mentioning

confidence: 99%

Exploratory examination of inflammation state, immune response and blood cell composition in a human obese cohort to identify potential markers predicting cancer risk

et al. 2020

View full text Add to dashboard Cite

show abstract

“…IVIG also normalizes the functions of DCs and other innate immune cells [43,77,78]. Further, IVIG induces expansion of regulatory T cells (Tregs) and reciprocally inhibits Th17 cells [79,80,89,[81][82][83][84][85][86][87][88]. Interestingly, recent studies in mouse models suggest that α-(2, 6) sialylated Fc of IVIG signals through type II lectin receptors to enhance inhibitory FcγRIIB on effector macrophages via basophil-secreted IL-4 and induce Tregs by dendritic cell-specific intercellular adhesion mol-ecule-3-grabbing nonintegrin (DC-SIGN)induced IL-33 secretion [90,91].…”

Section: Natural Igg (Nigg): Role Of Nabs In Immune Tolerance/homeostmentioning

confidence: 99%

“…Interestingly, recent studies in mouse models suggest that α-(2, 6) sialylated Fc of IVIG signals through type II lectin receptors to enhance inhibitory FcγRIIB on effector macrophages via basophil-secreted IL-4 and induce Tregs by dendritic cell-specific intercellular adhesion mol-ecule-3-grabbing nonintegrin (DC-SIGN)induced IL-33 secretion [90,91]. However, translation of these findings to humans failed to recapitulate the mechanisms although requirement of sialylation has been confirmed in other experimental models [78,79,82,83,88,89,92]. Studies in humans have revealed that IVIG can directly interact with basophils to induce IL-4 secretion, and can act either directly on Tregs or on DCs to expand Tregs [46,65,[93][94][95][96].…”

Section: Natural Igg (Nigg): Role Of Nabs In Immune Tolerance/homeostmentioning

confidence: 99%

Natural Antibodies: from First-Line Defense Against Pathogens to Perpetual Immune Homeostasis

Maddur

Lacroix‐Desmazes

Dimitrov

et al. 2019

Clinic Rev Allerg Immunol

Self Cite

View full text Add to dashboard Cite

show abstract

“…IVIG exerts beneficial effects via several mutually nonexclusive mechanisms. These mechanisms include: inhibiting activation of innate cells such as DCs, macrophages, monocytes and neutrophils and of inflammatory mediators secretion; modulation of B cell responses and inhibition of autoantibody production; suppression of pathogenic Th1 and Th17 cells and reciprocal enhancement of Tregs; and inhibition of endothelial cell and complement activation [45][46][47][48][49][50][51][52][53][54][55][56][57][58]. Although all these mechanisms might not be applicable to KD, several of them have been demonstrated in KD patients following IVIG therapy ( Table 2).…”

Section: Therapeutic Intervention Standard Therapymentioning

confidence: 99%

Predisposing factors, pathogenesis and therapeutic intervention of Kawasaki disease

Galeotti

Kaveri

Cimaz

et al. 2016

Drug Discovery Today

Self Cite

View full text Add to dashboard Cite

Kawasaki disease (KD) is an acute febrile childhood inflammatory disease, associated with coronary artery abnormalities. The disease is believed to result from an aberrant inflammatory response to an infectious trigger in a genetically predisposed individual. KD is associated with an endothelial cell injury as a consequence of T cell activation and cytotoxic effects of various proinflammatory cytokines. Intravenous immunoglobulin (IVIG) infusion and aspirin are the standard treatment of acute KD. However, 10-20% of patients show resistance to IVIG therapy and present higher risk of coronary vasculitis. The relative roles of second IVIG infusion, corticosteroids, calcineurin inhibitors, interleukin-1 antagonists and anti-tumor necrosis factor agents remain uncertain. In this review, we highlight the predisposing factors, pathogenesis and therapeutic intervention of KD, particularly new therapeutics for IVIG-resistant patients.

show abstract

Intravenous immunoglobulin-mediated expansion of regulatory T cells in autoimmune patients is associated with increased prostaglandin E2 levels in the circulation

Cited by 35 publications

References 10 publications

Exploratory examination of inflammation state, immune response and blood cell composition in a human obese cohort to identify potential markers predicting cancer risk

Exploratory examination of inflammation state, immune response and blood cell composition in a human obese cohort to identify potential markers predicting cancer risk

Natural Antibodies: from First-Line Defense Against Pathogens to Perpetual Immune Homeostasis

Predisposing factors, pathogenesis and therapeutic intervention of Kawasaki disease

Contact Info

Product

Resources

About