A migratory population of skin-derived dendritic cells expresses CXCR5, responds to B lymphocyte chemoattractantin vitro, and co-localizes to B cell zones in lymph nodesin vivo

Saeki, Hidehisa; Wu, Meng; Olasz, Edit; Hwang, Samuel T

doi:10.1002/1521-4141(200010)30:10<2808::aid-immu2808>3.0.co;2-k

Cited by 68 publications

(46 citation statements)

References 28 publications

(35 reference statements)

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“…In contrast, as discussed above, OX40L was not required. Expression of CXCR5, the marker of a DC subset found in B cell follicles and that has been implicated with induction of Th2 responses (22,46,47), was low on both Nb-loaded and other DC. Our in vivo studies using B cell-deficient mice showed that B cells are not required for the priming of IL-4-producing T cells and for Th2 responses to N. brasiliensis (48), again suggesting that B cell follicles and the associated cell populations are unlikely to be critical for IL-4 priming.…”

Section: Discussionmentioning

confidence: 99%

Helminth-Conditioned Dendritic Cells Prime CD4+ T Cells to IL-4 Production In Vivo

Connor

Tang

Camberis

et al. 2014

The Journal of Immunology

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Dendritic cells (DC) are critical for the initiation of immune responses; however, their role in priming IL-4–producing Th2 cells in vivo is not fully understood. We used a model of intradermal injection with fluorescent-labeled, nonviable larvae from the helminth parasite nonviable Nippostrongylus brasiliensis L3 larvae (Nb), a strong inducer of Th2 responses, together with IL-4–GFP reporter mice that enable a sensitive detection of IL-4 production to examine the contribution of DC to the priming of IL-4–producing CD4+ T cells in vivo. We found that parasite material is taken up by two distinct DC populations in draining lymph nodes: a mostly CD11cintMHC class II (MHCII)hiCD11b+Ly6C− dermal DC population and a CD11chiMHCIIintCD11b+Ly6C+ monocyte-derived DC population. After Nb treatment, these two DC populations appeared in the draining lymph nodes in comparable numbers and with similar kinetics; however, treatment with pertussis toxin blocked the migration of dermal DC and the priming of IL-4–producing T cells, but only partially affected monocyte-derived DC numbers. In line with this observation, transfer of OVA-loaded CD11cintMHCIIhi DC from Nb-treated mice into naive hosts could sensitize OVA-specific CD4+ T cells to IL-4 production, whereas transfer of CD11cintMHCIIhi DC from naive mice, or CD11chiMHCIIint DC from Nb-treated or naive mice, induced CD4+ T cell expansion but no IL-4 production. Phenotypic analysis of Nb-loaded CD11cintMHCIIhi DC revealed expression of programmed death ligand 2, CD301b, IFN regulatory factor 4, and moderate upregulation of OX40 ligand. However, thymic stromal lymphopoietin and OX40 ligand were not required for Th2 priming. Thus, our data suggest that appropriate stimuli can induce DC to express the unique signals sufficient to direct CD4+ T cells to Th2 differentiation.

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Section: Discussionmentioning

confidence: 99%

Helminth-Conditioned Dendritic Cells Prime CD4+ T Cells to IL-4 Production In Vivo

Connor

Tang

Camberis

et al. 2014

The Journal of Immunology

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“…These chemokines are fundamentally different in that CXCL9/Mig is induced by IFN-␥ 13 and recruits CXCR3 ϩ T-helper (Th) 1 and T-cytotoxic 1 cells, 14 whereas BLC/B-cell attracting 1/CXCL13 is constitutively expressed and recruits CXCR5 ϩ B and T lymphocytes and DCs to germinal centers. [15][16][17] Although signal intensities of approximately half of the chemokine mRNAs were at or below the limits of sensitivity of the assay (Table 2), this was not due to nucleotide-sequence heterogeneity between the rhesus macaque and human genes, since we have cloned and sequenced more than For personal use only. on April 5, 2019. by guest www.bloodjournal.org From homologous to their human counterparts (data not shown).…”

Section: Array Hybridization Identifies Cxcl9/mig Up-regulation In Spmentioning

confidence: 99%

Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-γ in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome

Reinhart

Fallert

Pfeifer

et al. 2002

Blood

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“…Homeostatic chemokines, such as CXCL13, CCL21, and CCL19, as well as their corresponding receptors, CXCR5 and CCR7, have been shown to closely cooperate in the development of lymphoid organs and the maintenance of lymphoid tissue microarchitecture (2). Expression of CXCR5 can be detected on mature recirculating B cells, small subsets of normal CD4 ϩ and CD8 ϩ T cells, and skin-derived migratory dendritic cells (3)(4)(5)(6). CXCR5 is essentially responsible for guiding B cells into the B cell zones of secondary lymphoid organs (7)(8)(9).…”

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confidence: 99%

CXC Chemokine Ligand 13 and CC Chemokine Ligand 19 Cooperatively Render Resistance to Apoptosis in B Cell Lineage Acute and Chronic Lymphocytic Leukemia CD23+CD5+ B Cells

et al. 2006

The Journal of Immunology

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CXCL13/CXCR5 and CCL19/CCR7 play a quite important role in normal physiological conditions, but the functions of both chemokine/receptor pairs in pathophysiological events are not well-investigated. We have investigated expression and functions of CXCL13/CXCR5 and CCL19/CCR7 in CD23+CD5+ and CD23+CD5− B cells from cord blood (CB) and patients with B cell lineage acute or chronic lymphocytic leukemia (B-ALL or B-CLL). CXCR5 and CCR7 are selectively expressed on B-ALL, B-CLL, and CB CD23+CD5+ B cells at high frequency, but not on CD23+CD5− B cells. Although no significant chemotactic responsiveness was observed, CXCL13 and CCL19 cooperatively induce significant resistance to TNF-α-mediated apoptosis in B-ALL and B-CLL CD23+CD5+ B cells, but not in the cells from CB. B-ALL and B-CLL CD23+CD5+ B cells express elevated levels of paternally expressed gene 10 (PEG10). CXCL13 and CCL19 together significantly up-regulate PEG10 expression in the same cells. We have found that CXCL13 and CCL19 together by means of activation of CXCR5 and CCR7 up-regulate PEG10 expression and function, subsequently stabilize caspase-3 and caspase-8 in B-ALL and B-CLL CD23+CD5+ B cells, and further rescue the cells from TNF-α-mediated apoptosis. Therefore, we suggest that normal lymphocytes, especially naive B and T cells, use CXCL13/CXCR5 and CCL19/CCR7 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis. In addition, certain malignant cells take advantages of CXCL13/CXCR5 and CCL19/CCR7 for infiltration, resistance to apoptosis, and inappropriate proliferation.

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A migratory population of skin-derived dendritic cells expresses CXCR5, responds to B lymphocyte chemoattractantin vitro, and co-localizes to B cell zones in lymph nodesin vivo

Cited by 68 publications

References 28 publications

Helminth-Conditioned Dendritic Cells Prime CD4+ T Cells to IL-4 Production In Vivo

Helminth-Conditioned Dendritic Cells Prime CD4+ T Cells to IL-4 Production In Vivo

Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-γ in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome

CXC Chemokine Ligand 13 and CC Chemokine Ligand 19 Cooperatively Render Resistance to Apoptosis in B Cell Lineage Acute and Chronic Lymphocytic Leukemia CD23+CD5+ B Cells

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