C-reactive Protein

Black, Steve; Kushner, Irving; Samols, David

doi:10.1074/jbc.r400025200

Cited by 1,356 publications

(1,071 citation statements)

References 52 publications

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“…In addition, we demonstrated that CRP has a direct inhibitory effect on the endocytic capability of monocyte-derived DC, and this effect could be effectively blocked by anti-CRP Ab. Although other studies have shown that CRP can stimulate phagocytosis functions in macrophages [51], our results clearly show that endocytosis by DC is greatly impaired by CRP. Therefore, CRP not only inhibited DC differentiation but also directly impaired the antigen capture capacity of DC in this study.…”

Section: Discussioncontrasting

confidence: 80%

C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function

Zhang¹,

Becnel

Li³

et al. 2006

Eur J Immunol

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C-reactive protein (CRP) is an acute phase reactant protein considered to be the prototypic marker for inflammation and its associated diseases. However, little is known about how CRP affects the immune system. In this study, we investigated the effect of CRP on dendritic cell (DC) differentiation, activation and biological functions. CD14 + monocytes were purified from PBMC and differentiated into DC in vitro. CRP (10 lg/ mL) substantially down-regulated expression of DC-SIGN (CD209) and the costimulatory molecules CD40 and CD86 during DC differentiation. This inhibitory effect was more pronounced when CRP was added at the early stage (0-2 days) of DC differentiation. The inhibitory effect of CRP could be specifically blocked by an anti-CD32 Ab. In addition, CRP dramatically down-regulated expression of the antigenuptake molecules CD205 and CD206, resulting in reduced DC endocytosis. Furthermore, CRP down-regulated expression of the costimulatory molecules CD40, CD80 and CD86 as well as the DC maturation marker CD83 after lipopolysaccharideinduced DC maturation. CRP-treated DC also showed an inhibitory effect on allogeneic T cell proliferation in a mixed leukocyte reaction. CRP treatment of activated DC preferentially decreased production of the proinflammatory and inflammatory cytokines IL-6, IL-8, IL-12, TNF-a, MIP-1a, MIP-1b and MCP-1. This work reveals a new role for CRP in modulating the immune system by inhibiting DC differentiation, maturation and functions mainly through FccRIIa/CD32.

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Section: Discussioncontrasting

confidence: 80%

C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function

Zhang¹,

Becnel

Li³

et al. 2006

Eur J Immunol

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“…IL-6 is an important cytokine responsible for the acute phase inflammatory response. IL-6 is known to induce the production of C-reactive protein (37,38). C-reactive protein has been identified as an important predictor of coronary heart disease (39).…”

Section: Figurementioning

confidence: 99%

Saturated and Polyunsaturated Fatty Acids Reciprocally Modulate Dendritic Cell Functions Mediated through TLR4

Weatherill

Lee

Zhao

et al. 2005

The Journal of Immunology

274

204

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TLRs provide critical signals to induce innate immune responses in APCs such as dendritic cells (DCs) that in turn link to adaptive immune responses. Results from our previous studies demonstrated that saturated fatty acids activate TLRs, whereas n-3 polyunsaturated fatty acids inhibit agonist-induced TLR activation. These results raise a significant question as to whether fatty acids differentially modulate immune responses mediated through TLR activation. The results presented in this study demonstrate that the saturated fatty acid, lauric acid, up-regulates the expression of costimulatory molecules (CD40, CD80, and CD86), MHC class II, and cytokines (IL-12p70 and IL-6) in bone marrow-derived DCs. The dominant negative mutant of TLR4 or its downstream signaling components inhibits lauric acid-induced expression of a CD86 promoter-reporter gene. In contrast, an n-3 polyunsaturated fatty acid, docosahexaenoic acid, inhibits TLR4 agonist (LPS)-induced up-regulation of the costimulatory molecules, MHC class II, and cytokine production. Similarly, DCs treated with lauric acid show increased T cell activation capacity, whereas docosahexaenoic acid inhibits T cell activation induced by LPS-treated DCs. Together, our results demonstrate that the reciprocal modulation of both innate and adaptive immune responses by saturated fatty acid and n-3 polyunsaturated fatty acid is mediated at least in part through TLRs. These results imply that TLRs are involved in sterile inflammation and immune responses induced by nonmicrobial endogenous molecules. These results shed new light in understanding how types of dietary fatty acids differentially modulate immune responses that could alter the risk of many chronic diseases.

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“…Contrasting Approaches to the Study of Inflammation and Disease C-reactive protein (CRP) is a prototypical acute-phase protein and commonly measured biomarker of inflammation (2). The recent advent of highly sensitive laboratory assays for CRP has led to the discovery that chronic low-grade inflammation-levels of inflammation previously thought to be inconsequential-may contribute to the pathophysiology of a wide range of diseases of aging, including cardiovascular disease (CVD) (3), type 2 diabetes (4), metabolic syndrome (3), and late-life disability (5) as well as allcause mortality (6).…”

mentioning

confidence: 99%

Early environments and the ecology of inflammation

McDade

2012

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

185

154

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Recent research has implicated inflammatory processes in the pathophysiology of a wide range of chronic degenerative diseases, although inflammation has long been recognized as a critical line of defense against infectious disease. However, current scientific understandings of the links between chronic low-grade inflammation and diseases of aging are based primarily on research in high-income nations with low levels of infectious disease and high levels of overweight/obesity. From a comparative and historical point of view, this epidemiological situation is relatively unique, and it may not capture the full range of ecological variation necessary to understand the processes that shape the development of inflammatory phenotypes. The human immune system is characterized by substantial developmental plasticity, and a comparative, developmental, ecological framework is proposed to cast light on the complex associations among early environments, regulation of inflammation, and disease. Recent studies in the Philippines and lowland Ecuador reveal low levels of chronic inflammation, despite higher burdens of infectious disease, and point to nutritional and microbial exposures in infancy as important determinants of inflammation in adulthood. By shaping the regulation of inflammation, early environments moderate responses to inflammatory stimuli later in life, with implications for the association between inflammation and chronic diseases. Attention to the eco-logics of inflammation may point to promising directions for future research, enriching our understanding of this important physiological system and informing approaches to the prevention and treatment of disease.

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C-reactive Protein

Cited by 1,356 publications

References 52 publications

C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function

C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function

Saturated and Polyunsaturated Fatty Acids Reciprocally Modulate Dendritic Cell Functions Mediated through TLR4

Early environments and the ecology of inflammation

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C-reactive Protein

Cited by 1,356 publications

References 52 publications

C‐reactive protein impairs human CD14+ monocyte‐derived dendritic cell differentiation, maturation and function

C‐reactive protein impairs human CD14+ monocyte‐derived dendritic cell differentiation, maturation and function

Saturated and Polyunsaturated Fatty Acids Reciprocally Modulate Dendritic Cell Functions Mediated through TLR4

Early environments and the ecology of inflammation

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Product

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C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function

C‐reactive protein impairs human CD14⁺ monocyte‐derived dendritic cell differentiation, maturation and function