Molecular Cloning of a Novel Human CC Chemokine EBI1-ligand Chemokine That Is a Specific Functional Ligand for EBI1, CCR7

Yoshida, Ruriko; Imai, Toshio; Hieshima, Kunio; Kusuda, Jun; Baba, Masataka; Kitaura, Motoji; Nishimura, Miyuki; Kakizaki, Mayumi; Nomiyama, Hisayuki; Yoshie, Osamu

doi:10.1074/jbc.272.21.13803

Cited by 369 publications

(280 citation statements)

References 76 publications

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“…29 CXCR4-or CXCL12-deficient mice share perinatal lethality because of hematopoietic, cardiovascular, and nervous system development defects. 29,38 The CCR7-CCL21 system plays an important role in naive lymphocyte homing to secondary lymphoid organs, which is impaired by disruption of the CCR7 gene [54][55][56] and is required for typical lymphoid tissue localization of Th1-type lymphocytes. 56,57 Both CCR7 and CXCR4 participate in the recruitment of lymphocytes from blood, 30,54 but CXCR4 Ϫ lymphocytes develop and seed peripheral lymphoid tissues normally.…”

Section: Discussionmentioning

confidence: 99%

CD30 triggering by agonistic antibodies regulates CXCR4 expression and CXCL12 chemotactic activity in the cell line L540

Vinante

Rigo

Scupoli

et al. 2002

Blood

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IntroductionThe tumor necrosis factor receptor (TNFR) family includes molecules such as TNFR1, TNFR2, CD27, CD30, CD40, CD95, and OX40, which interact with a corresponding family of TNF-like cytokines 1,2 integrating signals of activation, proliferation, apoptosis, or differentiation, depending on cell type, specific receptor expression, coactivation signals, and mobilization of transduction molecules. 1-4 CD30, CD40, OX40, and CD95 at least have been involved in lymphoid differentiation and effector functions. 5 CD30, originally described as a marker of a number of lymphoma cells and reactive lymphoblasts, 6 is expressed by activated and memory T cells, 6-9 medullary thymocytes, 10,11 B cells, natural killer cells, and some nonhematologic cells. 12 Its expression by T cells is essentially dependent on activation involving IL-4 and CD28 signaling. 9,13 The IL-4 requirement is probably the reason for the association of CD30 expression with preferential Th0-and Th2-type immune responses in vitro 8 and in vivo. [14][15][16] Stimulation of CD30 by CD153 (CD30 ligand) leads to nuclear mobilization of NF-B complexes 17 while inducing a signal-coupled depletion of TRAF2, which increases the cell sensitivity to TNFR1-dependent apoptosis. 3 This dual signaling may explain the pleiotropic effects after CD30 stimulation in CD30 ϩ lymphoma cell lines 18 and T cells, the latter acquiring a Th2-type function, 19 associated with inhibitory functions, 20 based on impaired clonal expansion of T cells. 10,20,21 High levels of soluble CD30 or TNF-␣ in the sera of patients infected with human immunodeficiency virus (HIV-1) at diagnosis have been shown to be an independent prognostic indicator of disease progression, 22,23 and the suggested role of CD30 in HIV-1 infection 15 has been linked to its ability to promote HIV-1 shedding through NF-B activation in infected cells. 24 The role of CD30 in HIV-1 infection, 15,22 the preferential association of CD30 with compartmentalized lymphoid subsets during differentiation 11 and effector responses, 16 and the evidence that Th1 versus Th2 or naive versus primed T cells are distinguished by specific patterns of CD30 8 and chemokine receptor expression 25,26 suggest some kind of relationship between CD30 signals and chemokine function. Recently, Muta et al 27 reported that CD30 signals increased amounts of CCR7 mRNA in the YT lymphoma cell line. Actually, a number of CD30-related activities seem to integrate cellular functions driven by lymphoid chemokines, namely their prototypic member CXCL12 (SDF-1) and its receptor CXCR4 (CD184). 28 CXCL12 is expressed constitutively in various cell types [28][29][30] and is an efficient cell chemoattractant to specific sites. [30][31][32] CXCR4 is expressed by neutrophils, monocytes, naive T lymphocytes, thymocytes, mature and immature B cells, CD34 ϩ cells, 31,32 vascular endothelial cells, 33 and neurologic cells. 32 It has been implicated in platelet formation 34 and is a coreceptor for HIV-1 entry. 35 CD30 and CD153 are reasonable candidates for reg...

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Section: Discussionmentioning

confidence: 99%

CD30 triggering by agonistic antibodies regulates CXCR4 expression and CXCL12 chemotactic activity in the cell line L540

Vinante

Rigo

Scupoli

et al. 2002

Blood

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“…Homeostatic chemokines are abundantly expressed in primary and secondary lymphoid organs; nevertheless, data demonstrating precise in vivo concentrations are still missing. In vitro migration assays are widely used to assess the activity of both homeostatic and inflammatory chemokines indicating the potency of each protein.In vitro migration using cell lines stably expressing single human chemokine receptors demonstrated chemotactic activities at fairly high concentrations for the homeostatic chemokines CCL19 and CCL21 [16,29] as well as for the inflammatory chemokine CCL7 [39]. Even though inflammatory chemokines are rapidly induced upon pro-inflammatory stimuli, the gradient generated in the early phase of the immune response might not yet be sufficient for the recruitment of cells expressing the selective receptor, raising the question if the chemokine milieu could trigger the initial recruitment.…”

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confidence: 99%

“…Constitutively expressed chemokines act in primary and secondary lymphoid organs [16,17,26] and peripheral tissues [27,28]. The CCR7 ligands, CCL19 and CCL21 [29,30], are expressed in the T-cell area of secondary lymphoid organs as well as on high endothelial venules (HEV) [31] and orchestrate the migration of CCR7 1 cells. ''Inflammatory'' chemokines are induced upon inflammation and cytokine production (e.g.…”

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confidence: 99%

Synergy‐inducing chemokines enhance CCR2 ligand activities on monocytes

Kuscher¹,

Danelon²,

Paoletti³

et al. 2009

Eur J Immunol

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The migration of monocytes to sites of inflammation is largely determined by their response to chemokines. Although the chemokine specificities and expression patterns of chemokine receptors are well defined, it is still a matter of debate how cells integrate the messages provided by different chemokines that are concomitantly produced in physiological or pathological situations in vivo. We present evidence for one regulatory mechanism of human monocyte trafficking. Monocytes can integrate stimuli provided by inflammatory chemokines in the presence of homeostatic chemokines. In particular, migration and cell responses could occur at much lower concentrations of the CCR2 agonists, in the presence of chemokines (CCL19 and CCL21) that per se do not act on monocytes. Binding studies on CCR2 1 cells showed that CCL19 and CCL21 do not compete with the CCR2 agonist CCL2. Furthermore, the presence of CCL19 or CCL21 could influence the degradation of CCL2 and CCL7 on cells expressing the decoy receptor D6. These findings disclose a new scenario to further comprehend the complexity of chemokinebased monocyte trafficking in a vast variety of human inflammatory disorders.Key words: Chemokine receptors . Chemokines . Monocytes . Synergism IntroductionConcomitant exposure to multiple chemokines, the key controllers of several immune cell functions [1], can result in enhancement of immune responses. Only recently, a broad phenomenon known as ''chemokine synergism'' has been identified [2][3][4][5][6][7][8][9][10]. Cells expressing two or more chemokine receptors, in the presence of the selective agonists, can amplify their response [2][3][4][5][6]11]. The responses mediated by low agonist concentrations can be powerfully enhanced by non-ligand chemokines in cells that do not bear the second chemokine receptor [7][8][9]. Using different biochemical approaches, these studies demonstrated that CC and CXC chemokines form heteromeric complexes, which could endow the agonist with higher activity [7,9,12].Chemokines mediate their effects through interactions with heterotrimeric G-protein-coupled receptors [13][14][15]. Most leukocytes express more than one chemokine receptor and, hence, can respond to more than one chemokine. Additionally, a great variety of in situ experiments demonstrated the concomitant expression of chemokines at target sites of leukocyte trafficking and homing [16][17][18][19][20][21].Many chemokines, apart from being agonistic for their receptors, were shown to act as natural antagonists on one or several receptors in vitro and in vivo [22]. Naturally occurring N-terminal truncations of chemokines have been identified in vivo [23] and numerous enzymes were shown to generate truncations of chemokines that render them less active or inactive [24,25]. Therefore, there are strong indications that a cell needs to 1118integrate more than one signal provided by its environment and that environmental factors other than agonists might influence their responses.Chemokine production can be either constitutive or triggere...

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“…Naive T cells, expressing the chemokine receptor CCR7, bind their ligands secondary lymphoid tissue chemokine (also called 6Ckine or CCL21) and EBV-induced molecule 1 ligand chemokine (CCL19), found in the T cell zone of the LN, and these receptor-ligand interactions are crucial for T cell homing to the LN (4,5). Following initial activation of T cells, CCR7 is down-modulated and CXCR5 expression is up-regulated, promoting T cell migration to the B lymphocyte-rich follicle expressing the B lymphocyte chemoattractant ligand (CXCL13) (6).…”

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confidence: 99%

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

Bai

Liu

Wang

et al. 2002

The Journal of Immunology

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Maneuvers that interfere with signals 1, 2, 3, or Ag processing can result in indefinite allograft survival. However, they are not applicable to all tissues, strains, or species, suggesting that there are additional levels of immune regulation. We hypothesized that secondary lymphoid organs are important for interactions among lymphocytes, alloantigen, and immunosuppressants that lead to tolerance. To explore this, cardiac allografts were performed with a tolerogenic immunosuppressive regimen. Concurrent administration of anti-L-selectin (CD62L) Ab, which prevents lymph node homing, prevents indefinite allograft survival and tolerance. Anti-CD62L Ab is not costimulatory, and Fab and F(ab′)2 anti-CD62L have similar activities. Flow cytometry and histologic examination show that Ab shifts T cells away from lymph nodes and into spleen, peripheral blood, and graft. Tolerance is not induced in CD62L−/− mice, and adoptive transfer of CD62L−/−, but not CD62L+/+, T cells prevents tolerization in wild-type recipients. FTY720, an immunosuppressant that promotes chemokine-dependent, but CD62L-independent, lymph node homing, reverses the Ab effect. Blockade of other homing receptors also prevents tolerization. These results indicate that T lymphocytes use CD62L-dependent migration for alloantigen-specific tolerance, and suggest that lymph nodes or other lymphoid tissues are an important site for peripheral tolerization to alloantigen.

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Molecular Cloning of a Novel Human CC Chemokine EBI1-ligand Chemokine That Is a Specific Functional Ligand for EBI1, CCR7

Cited by 369 publications

References 76 publications

CD30 triggering by agonistic antibodies regulates CXCR4 expression and CXCL12 chemotactic activity in the cell line L540

CD30 triggering by agonistic antibodies regulates CXCR4 expression and CXCL12 chemotactic activity in the cell line L540

Synergy‐inducing chemokines enhance CCR2 ligand activities on monocytes

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

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