IL-10 Induces CCR6 Expression During Langerhans Cell Development While IL-4 and IFN-γ Suppress It

Dieu-Nosjean, Marie-Caroline; Massacrier, Catherine; Vanbervliet, Béatrice; Fridman, Wolf‐Herman; Caux, Christophe

doi:10.4049/jimmunol.167.10.5594

Cited by 41 publications

(26 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IL-10-conditioned iDC were previously shown to be resistant to maturation (36) and to display deregulated chemokine receptor patterns with low CCR7 levels (37,38). The upshot of these characteristics is the induction of Ag-specific T cell anergy (3).…”

Section: Cd14mentioning

confidence: 99%

A Postmigrational Switch among Skin-Derived Dendritic Cells to a Macrophage-Like Phenotype Is Predetermined by the Intracutaneous Cytokine Balance

Gruijl¹,

Sombroek

Lougheed³

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

Migration of dendritic cells (DC) to secondary lymphoid organs under proinflammatory conditions coincides with their maturation and acquisition of T cell stimulatory abilities. In contrast, impaired activation of DC, e.g., in tumor-conditioned environments, may hamper their activation and possibly their subsequent migration to lymph nodes, leading to either immunological tolerance or ignorance, respectively. In this study, the influence of cytokines in the peripheral skin microenvironment on the activation state of migrating cutaneous DC was assessed using an ex vivo human skin explant model. We observed a phenotypic shift from mature CD83+ DC to immature CD14+ macrophage-like cells within 7 days subsequent to migration from unconditioned skin. These macrophage-like cells displayed a poor T cell stimulatory ability and lacked expression of CCR7, thus precluding their migration to paracortical T cell areas in the lymph nodes. The balance of suppressive and stimulatory cytokines during the initiation of migration decided the postmigrational fate of DC with IL-10 accelerating and GM-CSF and IL-4 preventing the phenotypic switch, which proved irreversible once established. These observations indicate that, in immunosuppressed environments, a postmigrational DC-to-macrophage shift may hinder T cell activation, but also that it may be prevented by prior conditioning of the tissue microenvironment by GM-CSF and/or IL-4.

show abstract

Section: Cd14mentioning

confidence: 99%

A Postmigrational Switch among Skin-Derived Dendritic Cells to a Macrophage-Like Phenotype Is Predetermined by the Intracutaneous Cytokine Balance

Gruijl¹,

Sombroek

Lougheed³

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…DC migration was evaluated using a chemotaxis microchamber technique (48-well Boyden microchamber; NeuroProbe) as previously described (12). Briefly, chemokines were diluted and added to the lower wells of the FIGURE 1.…”

Section: Chemotaxis Assaysmentioning

confidence: 99%

CCL1-CCR8 Interactions: An Axis Mediating the Recruitment of T Cells and Langerhans-Type Dendritic Cells to Sites of Atopic Skin Inflammation

Gombert

Dieu-Nosjean

Winterberg

et al. 2005

The Journal of Immunology

Self Cite

185

142

View full text Add to dashboard Cite

Atopic dermatitis represents a chronically relapsing skin disease with a steadily increasing prevalence of 10–20% in children. Skin-infiltrating T cells, dendritic cells (DC), and mast cells are thought to play a crucial role in its pathogenesis. We report that the expression of the CC chemokine CCL1 (I-309) is significantly and selectively up-regulated in atopic dermatitis in comparison to psoriasis, cutaneous lupus erythematosus, or normal skin. CCL1 serum levels of atopic dermatitis patients are significantly higher than levels in healthy individuals. DC, mast cells, and dermal endothelial cells are abundant sources of CCL1 during atopic skin inflammation and allergen challenge, and Staphylococcus aureus-derived products induce its production. In vitro, binding and cross-linking of IgE on mast cells resulted in a significant up-regulation of this inflammatory chemokine. Its specific receptor, CCR8, is expressed on a small subset of circulating T cells and is abundantly expressed on interstitial DC, Langerhans cells generated in vitro, and their monocytic precursors. Although DC maintain their CCR8+ status during maturation, brief activation of circulating T cells recruits CCR8 from intracytoplamic stores to the cell surface. Moreover, the inflammatory and atopy-associated chemokine CCL1 synergizes with the homeostatic chemokine CXCL12 (SDF-1α) resulting in the recruitment of T cell and Langerhans cell-like DC. Taken together, these findings suggest that the axis CCL1-CCR8 links adaptive and innate immune functions that play a role in the initiation and amplification of atopic skin inflammation.

show abstract

“…Previous reports indicated that the chemotactic responses of cells toward chemokines could be affected by other cytokines as a result of modulation of chemokine receptor expression on the cell surface. 34,35 To determine whether CCL2/JE-induced inhibition of SDF-1 chemotaxis was caused by altered cell surface expression of the CXCR4 receptor, we examined CXCR4 receptor expression on immature B cells pretreated in the presence or absence of JE/CCL2. As shown in Figure 5C, CCL2 did not alter the level of CXCR4 expression on B cells.…”

Section: Ccr2-induced Inhibitory Pathway Is Ifn-␥ Independentmentioning

confidence: 99%

Expression of the chemokine receptor CCR2 on immature B cells negatively regulates their cytoskeletal rearrangement and migration

Flaishon

Becker-Herman

Hart

et al. 2004

Blood

View full text Add to dashboard Cite

In the bone marrow, B-cell development can be divided into different stages according to the rearrangement status of the immunoglobulin H (IgH) and IgL chain loci 1,2 and the expression of intracellular and surface-bound markers. The first cells expressing IgM at their surface during this developmental process are the immature B cells, 3 which leave the bone marrow and migrate to the spleen for their final maturation. 4,5 One of the most fundamental and important aspects of the immune system is its ability to recognize and respond to virtually any foreign antigen while maintaining strict unresponsiveness to self-antigens. For B cells, antigens encountered during the immature stage are likely to be self-antigens, and reactive clones are, therefore, subjected to negative selection through deletion, [6][7][8] receptor editing, 9,10 and anergy. 11 The selection process occurring within the immature B-cell compartments is also extended to the periphery, allowing deletion of virtually all B cells recognizing peripheral self-antigens outside of the bone marrow. 12 Immature B cells leave the bone marrow and migrate to the spleen where they can mature prior to antigen encounter. Like other naive lymphocytes, before their arrival in the spleen immature B cells might recirculate to nonsplenic secondary lymphoid organs, which are specialized tissues for collecting antigens, 13 or to sites of infection and inflammation. In these secondary lymphoid organs, where differentiation to mature cells does not occur, antigen encounter would lead to the death of the immature B cells and elimination of effective clones because of the negative selection process. Thus, it is imperative for B cells to home to the spleen and undergo a splenic maturation step before their release into the periphery.Homing of immature B cells to the spleen proceeds through the terminal branches of central arterioles to blood sinusoids of the marginal zone. 4,14 These immature B cells then penetrate the marginal zone sinus and reside in the outer zone of the periarteriolar lymphoid sheath (PALS), 15 where they become part of the B-cell-rich follicular areas. 15,16 At this site in the spleen, B cells are still immature and can be distinguished from their mature counterparts. 4,14,17 The transition from immature to mature B cell is characterized by a series of changes in surface marker expression and the activities of these B cells.Two populations of splenic B cells were recently identified as precursors of mature cells. Transitional B cells of type 1 (T1) are the recent immigrants from the bone marrow. Migrating T1 cells expressing B-cell receptors (BCRs) with high affinity to soluble self-antigens (Ags) in the blood are likely to die by negative selection by way of Ag-induced death. On entry to the spleen, T1 cells remain at the PALS, where additional bloodborne self-Ags trapped by the spleen may further drive negative selection. The remaining T1 cells develop into transitional B cells of type 2 (T2), which are found exclusively in the primary follicles of th...

show abstract

IL-10 Induces CCR6 Expression During Langerhans Cell Development While IL-4 and IFN-γ Suppress It

Cited by 41 publications

References 69 publications

A Postmigrational Switch among Skin-Derived Dendritic Cells to a Macrophage-Like Phenotype Is Predetermined by the Intracutaneous Cytokine Balance

A Postmigrational Switch among Skin-Derived Dendritic Cells to a Macrophage-Like Phenotype Is Predetermined by the Intracutaneous Cytokine Balance

CCL1-CCR8 Interactions: An Axis Mediating the Recruitment of T Cells and Langerhans-Type Dendritic Cells to Sites of Atopic Skin Inflammation

Expression of the chemokine receptor CCR2 on immature B cells negatively regulates their cytoskeletal rearrangement and migration

Contact Info

Product

Resources

About