Production of the RANTES chemokine in delayed-type hypersensitivity reactions: involvement of macrophages and endothelial cells.

Devergne, Odile; Marfaing-Koka, Anne; Schall, Thomas J.; Leger-Ravet, M.B.; Sadick, Michael D.; Peuchmaur, Michel; Crevon, Marie‐Claude; Kim, K J; Schall, Thomas; Kim, T

doi:10.1084/jem.179.5.1689

Cited by 200 publications

(119 citation statements)

References 34 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…Only a few studies have examined the induction of genes for MCP-3, MIP-1b and I-309 (TCA3) in diseased states, but MIP-1a and RANTES have been shown to be involved in several diseases [26][27][28][29][30][31][32][33][34][35]. In glomerular diseases, Tang et al [23] demonstrated that expression of genes for MCP-1 and MIP-1a, but not for RANTES, was enhanced in a non-crescentic anti-GBM model.…”

Section: Discussionmentioning

confidence: 99%

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Natori¹,

Sekiguchi²,

Ou³

et al. 1997

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYCGN is a rapidly progressive glomerular disease. Monocytes/macrophages are frequently observed in glomeruli in cases of CGN and they are considered to play a crucial role in the pathogenesis of this disease. We described previously the glomerular expression of monocyte chemoattractant protein-1 (MCP-1), which is a potent chemoattractant for monocytes and a member of CC chemokine family, in an experimental model of CGN. In the present study we investigated the expression of mRNAs for other CC chemokines, namely, MCP-3, macrophage inflammatory protein-1a (MIP-1a), MIP-1b, RANTES and TCA3, all of which are chemotactic for monocytes, in the CGN model. First, we established a reverse transcriptase-polymerase chain reaction (RT-PCR) method by which mRNA for each of the CC chemokines could be amplified separately, and then we measured the levels of the expression of mRNAs for the chemokines in diseased glomeruli at several time points after induction of CGN. The mRNAs for all CC chemokines examined were expressed in glomeruli of rats with CGN. Moreover, induction of the gene expression of MIP-1a and MIP-1b seemed to occur earlier than that of the others. CC chemokines may contribute to the recruitment and activation of monocytes in CGN, and each individual CC chemokine may play an overlapping but distinct role in the pathogenesis of this disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Natori¹,

Sekiguchi²,

Ou³

et al. 1997

Clinical and Experimental Immunology

View full text Add to dashboard Cite

show abstract

“…RANTES has been shown to play a role in DTH responses, but would normally be considered pro-inflammatory (Devergne et al 1994). The reduction in local levels of RANTES in response to OVX (i.e.…”

Section: Discussionmentioning

confidence: 99%

Local cytokine levels associated with delayed-type hypersensitivity responses: modulation by gender, ovariectomy, and estrogen replacement

Lisa

Guzmán

Muller

et al. 2007

Journal of Endocrinology

View full text Add to dashboard Cite

It is well established that females mount stronger immune responses than males, but only very little is understood about the underlying mechanisms. We have analyzed local cytokine differences among intact females, those that had been ovariectomized (OVX), those receiving estrogen replacement after OVX, and males, both before and after production of delayed-type hypersensitivity (DTH) responses. We report confirmation of a much larger DTH response in females versus males. However, OVX resulted in an even larger response, while estrogen replacement resulted in a smaller response when compared with intact females. In animals exposed for the first time to an antigen (without a DTH response), OVX increased interleukin-6 (IL-6) and estrogen replacement after OVX suppressed IL-6. Of the cytokines that differed between males and females exposed for the first time to an antigen, only IL-6 was higher in females versus males when exposure to antigen occurred for the second time (when the DTH response occurs). Analysis of cytokines with OVX and estrogen replacement after a second exposure to antigen showed that IL-6 did not significantly change. Levels of IL-4; Regulated upon Activation, Normal T-cell Expressed; and Secreted; and thrombopoietin, however, correlated with the DTH response, suggesting direct or indirect positive regulation by estrogen. These results suggest an important role for both IL-6 and IL-4 in determining the degree of DTH response, with IL-6 (which appears negatively regulated by estrogen) increasing and IL-4 (which appears positively regulated by estrogen) decreasing the response. The results further suggest that IL-6 may play a role in predisposing to a larger DTH response, while IL-4 levels seem more important during an active response.

show abstract

“…17 Chemokines are a large family of soluble molecules expressed by ECs, smooth muscle cells, or lymphocytes that attract, and in many cases activate, a variety of inflammatory and noninflammatory cells. 18,19 Chronic allograft endothelial injury leads to macrophage migration, as well as the eventual accumulation and proliferation of intimal smooth muscle-like cells. 19 -21 To date, more than 50 chemokines have been identified.…”

Section: Discussionmentioning

confidence: 99%

Direct Anti-Inflammatory Mechanisms Contribute to Attenuation of Experimental Allograft Arteriosclerosis by Statins

et al. 2003

View full text Add to dashboard Cite

Background-Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. The interplay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic lesion, which leads to ischemia and graft failure. HMG-CoA reductase inhibitors (statins) reduce GAD in human cardiac allografts, although it is unclear whether this is secondary to cholesterol lowering or other mechanisms. This study tested the hypothesis that statins can suppress GAD by cholesterol-independent pathways. Methods and Results-We performed heterotopic murine cardiac transplants in total allogeneic or major histocompatibility complex class II-mismatched combinations. Transplanted animals received either control chow, chow containing 25 ppm cerivastatin (low dose), or chow containing 125 ppm cerivastatin (high dose). Mean plasma cerivastatin concentrations were 0.0 (control), 10.1 (low dose), and 21.9 (high dose) nmol/L, respectively. Plasma cholesterol levels were the same in all groups. GAD scores decreased in low-dose (PϽ0.05) and high-dose (PϽ0.0001) cerivastatin groups compared with controls, with concomitant reduction in graft-infiltrating cells and significantly decreased intragraft RANTES and monocyte chemotactic protein-1 mRNA expression. Cerivastatin, as well as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endothelial cells stimulated with interferon-␥ and tumor necrosis factor-␣ in vitro. Conclusions-Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine heart transplants, diminish host inflammatory cell recruitment, and do not alter cholesterol levels.

show abstract

Production of the RANTES chemokine in delayed-type hypersensitivity reactions: involvement of macrophages and endothelial cells.

Cited by 200 publications

References 34 publications

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)

Local cytokine levels associated with delayed-type hypersensitivity responses: modulation by gender, ovariectomy, and estrogen replacement

Direct Anti-Inflammatory Mechanisms Contribute to Attenuation of Experimental Allograft Arteriosclerosis by Statins

Contact Info

Product

Resources

About