The Dendritic Cell-Specific Chemokine, Dendritic Cell-Derived CC Chemokine 1, Enhances Protective Cell-Mediated Immunity to Murine Malaria

Bruña–Romero, Oscar; Schmieg, John; Val, Margarita Del; Buschle, Michael; Tsuji, Moriya

doi:10.4049/jimmunol.170.6.3195

Cited by 32 publications

(18 citation statements)

References 58 publications

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“…Furthermore, CCL18 is chemotactic for T cells (30) suggesting that this chemokine plays a role in the organization of T cell responses. This idea is supported by a recent study demonstrating that human CCL18 enhanced Ag-specific primary CD8 ϩ T cell responses when coadministered with malaria vaccines in mice (31). In this study, we report that CCL18 was absent in the normal skin of healthy individuals and in the nonlesional skin of atopic individuals but showed abundant expression in lesional atopic dermatitis.…”

Section: Discussionsupporting

confidence: 77%

CC Chemokine Ligand 18, An Atopic Dermatitis-Associated and Dendritic Cell-Derived Chemokine, Is Regulated by Staphylococcal Products and Allergen Exposure

Pivarcsi¹,

Gombert²,

Dieu-Nosjean

et al. 2004

The Journal of Immunology

110

117

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Atopic dermatitis is a chronic inflammatory skin disease with a steadily increasing prevalence. Exposure to allergens or bacterial superantigens triggers T and dendritic cell (DC) recruitment and induces atopic skin inflammation. In this study, we report that among all known chemokines CCL18/DC-CK1/PARC represents the most highly expressed ligand in atopic dermatitis. Moreover, CCL18 expression is associated with an atopic dermatitis phenotype when compared with other chronic inflammatory skin diseases. DCs either dispersed within the dermis or clustering at sites showing perivascular infiltrates are abundant sources of CCL18. In vitro, microbial products including LPS, peptidoglycan, and mannan, as well as the T cell-derived activation signal CD40L, induced CCL18 in monocytes. In contrast to monocytes, monocyte-derived, interstitial-type, and Langerhans-type DCs showed a constitutive and abundant expression of CCL18. In comparison to Langerhans cells, interstitial-type DCs produced higher constitutive levels of CCL18. In vivo, topical exposure to the relevant allergen or the superantigen staphylococcal enterotoxin B, resulted in a significant induction of CCL18 in atopic dermatitis patients. Furthermore, in nonatopic NiSO4-sensitized individuals, only relevant allergen but not irritant exposure resulted in the induction of CCL18. Taken together, findings of the present study demonstrate that CCL18 is associated with an atopy/allergy skin phenotype, and is expressed at the interface between the environment and the host by cells constantly screening foreign Ags. Its regulation by allergen exposure and microbial products suggests an important role for CCL18 in the initiation and amplification of atopic skin inflammation.

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Section: Discussionsupporting

confidence: 77%

CC Chemokine Ligand 18, An Atopic Dermatitis-Associated and Dendritic Cell-Derived Chemokine, Is Regulated by Staphylococcal Products and Allergen Exposure

Pivarcsi¹,

Gombert²,

Dieu-Nosjean

et al. 2004

The Journal of Immunology

110

117

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“…The alternative macrophage activation-associated chemokine PARC/CCL18 is mainly produced by antigen-presenting cells induced by Th2 type cytokines and may exhibit dual functions, with pro-and anti-infl ammatory properties [43]. PARC/ CCL18 was found to enhance protective cell-mediated immunity in murine malaria suggesting this chemokine as a potential adjuvant to enhance adaptive immune responses against Plasmodium yoelii infection [44]. In our study, plasma levels of TARC/CCL17 and PARC/CCL18 were similarly high in children with severe malaria and in adults with uncomplicated malaria, suggesting that even though being diminished in children to adult levels, PARC and TARC may not be the critical components which mediate an immune response preventive against severe malaria.…”

Section: Discussionmentioning

confidence: 99%

Chemokine levels and parasite- and allergen-specific antibody responses in children and adults with severe or uncomplicatedPlasmodium falciparummalaria

Wangala¹,

Vovor²,

Gantin³

et al. 2015

European Journal of Microbiology and Immunology

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Chemokine a nd antibody response profiles were investigated in children and adults with severe or uncomplicated Plasmodium falciparum malaria; the aim was to reveal which profiles are associated with severe disease, as often seen in nonimmune children, or with mild and uncomplicated disease, as seen in semi-immune adults. Blood samples were obtained from children under 5 years of age as well as adults with falciparum malaria. Classification of malaria was performed according to parasite densities and hemoglobin concentrations. Plasma levels of chemokines (IL-8, IP-10, MCP-4, TARC, PARC, MIP-1δ, eotaxins) were quantified, and antibody responses (IgE, IgG1, and IgG4) to P. falciparum, Entamoeba histolytica-specific antigen, and mite allergen extracts were determined. In children with severe malaria proinflammatory, IL-8, IP10, MIP-1δ, and LARC were at highly elevated levels, suggesting an association with severe disease. In contrast, the Th2-type chemokines TARC, PARC, and eotaxin-2 attained in children the same levels as in adults suggesting the evolution of immune regulatory components. In children with severe malaria, an elevated IgG1 and IgE reactivity to mite allergens and intestinal protozoan parasites was observed. In conclusion, exacerbated proinflammatory chemokines together with IgE responses to mite allergens or E. histolytica-specific antigen extract were observed in children with severe falciparum malaria.

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“…Increased protection of mice was achieved by coadministration of dendritic cell-derived CC chemokine 1 with irradiated sporozoites (7). Earlier studies showed that IL-4-producing CD4 T cells in the liver were important for the development of a protective CD8 ϩ T-cell response against the malaria liver stage (8).…”

Section: Discussionmentioning

confidence: 99%

Mice Deficient in Interleukin-4 (IL-4) or IL-4 Receptor α Have Higher Resistance to Sporozoite Infection withPlasmodium berghei(ANKA) than Do Naive Wild-Type Mice

Saeftel

Krueger²,

Arriens³

et al. 2004

Infect Immun

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BALB/c interleukin-4 (IL-4؊/؊ ) or IL-4 receptor-␣ (IL-4r␣ ؊/؊ ) knockout (KO) mice were used to assess the roles of the IL-4 and IL-13 pathways during infections with the blood or liver stages of plasmodium in murine malaria. Intraperitoneal infection with the blood-stage erythrocytes of Plasmodium berghei (ANKA) resulted in 100% mortality within 24 days in BALB/c mice, as well as in the mutant mouse strains. However, when infected intravenously with the sporozoite liver stage, 60 to 80% of IL-4 ؊/؊ and IL-4r␣ ؊/؊ mice survived, whereas all BALB/c mice succumbed with high parasitemia. Compared to infected BALB/c controls, the surviving KO mice showed increased NK cell numbers and expression of inducible nitric oxide synthase (iNOS) in the liver and were able to eliminate parasites early during infection. In vivo blockade of NO resulted in 100% mortality of sporozoite-infected KO mice. In vivo depletion of NK cells also resulted in 80 to 100% mortality, with a significant reduction in gamma interferon (IFN-␥) production in the liver. These results suggest that IFN-␥-producing NK cells are critical in host resistance against the sporozoite liver stage by inducing NO production, an effective killing effector molecule against Plasmodium. The absence of IL-4-mediated functions increases the protective innate immune mechanism identified above, which results in immunity against P. berghei infection in these mice, with no major role for IL-13.Both cell-mediated immunity and humoral immunity play important roles in the mechanisms of defense against human and animal malaria. These defense mechanisms largely depend on early innate responses and antigen-specific T helper (Th) cell activation. The importance of the Th1 cytokine gamma interferon (IFN-␥) for protection against malaria has been shown in murine models of malaria (1,11,47,50,54,55,57), with vaccinated animals lacking IFN-␥ showing greatly increased susceptibility, increased parasitemia, and a shorter life span.The role of nitric oxide (NO) in the defense against malaria infection seems to be dependent on the stage of the malaria parasite. In a blood-stage infection with Plasmodium berghei, it was shown that neither NO nor NK cells were important for the control of parasitemia (12, 55). In contrast, compared to the liver-phase stage of sporozoite infection, NK cells were shown to be activated by sporozoites (37) and produced IFN-␥ (31, 37). A clear role for NO as a defense mechanism against the liver stage of P. berghei was found only in vaccinated animals (25,36,45,48).Concerning Th2 response, it was shown that a lack of interleukin-4 (IL-4) in the murine infection with Plasmodium chabaudi chabaudi results in a course of infection similar to that seen in the wild-type mice (2, 50, 51), with slightly different parasitemia kinetics. Moreover the in vitro Th1 immune responses were sustained in the IL-4-deficient mice (51). All of these studies were done by infection of mice with parasitized erythrocytes, but no study has been performed that focused on the role of I...

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The Dendritic Cell-Specific Chemokine, Dendritic Cell-Derived CC Chemokine 1, Enhances Protective Cell-Mediated Immunity to Murine Malaria

Cited by 32 publications

References 58 publications

CC Chemokine Ligand 18, An Atopic Dermatitis-Associated and Dendritic Cell-Derived Chemokine, Is Regulated by Staphylococcal Products and Allergen Exposure

CC Chemokine Ligand 18, An Atopic Dermatitis-Associated and Dendritic Cell-Derived Chemokine, Is Regulated by Staphylococcal Products and Allergen Exposure

Chemokine levels and parasite- and allergen-specific antibody responses in children and adults with severe or uncomplicatedPlasmodium falciparummalaria

Mice Deficient in Interleukin-4 (IL-4) or IL-4 Receptor α Have Higher Resistance to Sporozoite Infection withPlasmodium berghei(ANKA) than Do Naive Wild-Type Mice

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