Complex regulation of CCR9 at multiple discrete stages of T cell development

Wurbel, Marc‐André; Malissen, Bernard; Campbell, James J.

doi:10.1002/eji.200535203

Cited by 61 publications

(89 citation statements)

References 27 publications

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“…Thymic size and cellularity were comparable among WT, CCR9 Ϫ/Ϫ , and CCL25 Ϫ/Ϫ mice. As we reported previously (6,16), there were no differences in the relative proportions of these subsets between normal and CCR9-deficient mice (Fig. 3A).…”

Section: Thymic Phenotype Of Ccl25 ϫ/ϫ Micesupporting

confidence: 83%

“…Furthermore, new discoveries in the past year have shown that all naive murine CD8 T cells express functional CCR9 (6) and that recent thymic-emigrant CD8 T cells can colonize the gut in a CCR9-dependent manner (18,19). These findings suggest that the role of CCL25-CCR9 interactions in thymic development and intestinal memory are intertwined more extensively than previously believed.…”

Section: Impaired Accumulation Of Antigen-specific Cd8 Lymphocytes Inmentioning

confidence: 92%

“…In the thymus, CCL25-CCR9 interactions appear to play an important role in the migration of early T cells into the cortex from the subcapsular zone after successful TCR␤ gene rearrangement (4 -7). CCR9 may also play an earlier role in thymic development, either by directly controlling thymic colonization (8 -10) or by participating in thymic precursor development within the bone marrow (BM) 3 (6,11,12).…”

Section: Impaired Accumulation Of Antigen-specific Cd8 Lymphocytes Inmentioning

confidence: 99%

“…C57BL/6N (Charles River Laboratories), OT-1-transgenic (Tg) and B6.SJL-Ptprc a Pep3 b /BoyJ (The Jackson Laboratory) and CCL25-deficient (see below) and CCR9-deficient mice (6,16) were bred in the animal facility at the Children's Hospital (Boston, MA), and held under specific pathogen-free (SPF) conditions. All mouse procedures were approved by the Children's Hospital Institutional Animal Care and Use Committee.…”

Section: Micementioning

confidence: 99%

“…Six-color flow cytometry was performed on mice between 4 and 12 wk of age as described (6). Cell suspensions were prepared from WT, CCL25-deficient, and CCR9-deficient thymus, spleen (SPL), mesenteric lymph nodes (MLN), peripheral lymph nodes (PLN), Peyer's patches (PP), lamina propria (LP lymphocyte (LPL)), and epithelium (intraepithelial lymphocytes (IEL)) of the small intestine.…”

Section: Multicolor Flow Cytometry Analysismentioning

confidence: 99%

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Impaired Accumulation of Antigen-Specific CD8 Lymphocytes in Chemokine CCL25-Deficient Intestinal Epithelium and Lamina Propria

Wurbel

Malissen

Guy‐Grand

et al. 2007

The Journal of Immunology

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CCL25 and CCR9 constitute a chemokine/receptor pair involved in T cell development and in gut-associated immune responses. In this study, we generated CCL25−/− mice to answer questions that could not be addressed with existing CCR9−/− mice. Similar phenotypes were observed for both CCL25−/− and CCR9−/− mice, consistent with the notion that CCL25 and CCR9 interact with each other exclusively. We assessed the requirement for CCL25 in generating CCR9high CD8 intestinal memory-phenotype T cells and the subsequent accumulation of these cells within effector sites. TCR-transgenic naive CD8 T cells were transferred into wild-type or CCL25-deficient hosts. Oral sensitization with Ag allowed these naive donor cells to efficiently differentiate into CCR9high memory-phenotype cells within the mesenteric lymph nodes of wild-type hosts. This differentiation event occurred with equal efficiency in the MLN of CCL25-deficient hosts, demonstrating that CCL25 is not required to induce the CCR9high memory phenotype in vivo. However, we found that CCL25 deficiency severely impaired the Ag-dependent accumulation of donor-derived CD8 T cells within both lamina propria and epithelium of the small intestine. Thus, although CCL25 is not necessary for generating memory-phenotype CD8 T cells with “gut-homing” properties, this chemokine is indispensable for their trafficking to the small intestine.

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Section: Thymic Phenotype Of Ccl25 ϫ/ϫ Micesupporting

confidence: 83%

Section: Impaired Accumulation Of Antigen-specific Cd8 Lymphocytes Inmentioning

confidence: 92%

Section: Impaired Accumulation Of Antigen-specific Cd8 Lymphocytes Inmentioning

confidence: 99%

Section: Micementioning

confidence: 99%

Section: Multicolor Flow Cytometry Analysismentioning

confidence: 99%

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Impaired Accumulation of Antigen-Specific CD8 Lymphocytes in Chemokine CCL25-Deficient Intestinal Epithelium and Lamina Propria

Wurbel

Malissen

Guy‐Grand

et al. 2007

The Journal of Immunology

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The Role of Transferrin in Actinide(IV) Uptake: Comparison with Iron(III)

Jeanson¹,

Ferrand²,

Funke³

et al. 2010

Chemistry A European J

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The impact of actinides on living organisms has been the subject of numerous studies since the 1950s. From a general point of view, these studies show that actinides are chemical poisons as well as radiological hazards. Actinides in plasma are assumed to be mainly complexed to transferrin, the iron carrier protein. This paper casts light on the uptake of actinides(IV) (thorium, neptunium, plutonium) by transferrin, focusing on the pH dependence of the interaction and on a molecular description of the cation binding site in the protein. Their behavior is compared with that of iron(III), the endogenous transferrin cation, from a structural point of view. Complementary spectroscopic techniques (UV/Vis spectrophotometry, microfiltration coupled with gamma spectrometry, and X-ray absorption fine structure) have been combined in order to propose a structural model for the actinide-binding site in transferrin. Comparison of our results with data available on holotransferrin suggests some similarities between the behavior of Fe(III) and Np(IV)/Pu(IV)/ Np(IV) is not complexed at pH <7, whereas at pH approximately 7.4 complexation can be regarded as quantitative. This pH effect is consistent with the in vivo transferrin "cycle". Pu(IV) also appears to be quantitatively bound by apotransferrin at around pH approximately 7.5, whereas Th(IV) was never complexed under our experimental conditions. EXAFS data at the actinide edge have allowed a structural model of the actinide binding site to be elaborated: at least one tyrosine residue could participate in the actinide coordination sphere (two for iron), forming a mixed hydroxo-transferrin complex in which actinides are bound with transferrin both through An-tyrosine and through An--OH bonds. A description of interatomic distances is provided.

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Lymphocyte homing and its role in the pathogenesis of IBD

Eksteen

Liaskou

Adams

2008

Inflammatory Bowel Diseases

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Inflammatory bowel disease (IBD) is an idiopathic disorder of chronic inflammation of the gastrointestinal tract. Experimental models of IBD and results from human genomewide linkage studies suggest that the primary defect that leads to IBD is an inappropriate mucosal immune response to normal intestinal microbes. Genetic alterations not only confer increased susceptibility to IBD but also appear to determine the nature and location of the intestinal inflammation, as is evident in patients with genetic alterations of NOD2 and their susceptibility for ileal Crohn's disease. IBD has traditionally been classified into 2 subtypes, namely, ulcerative colitis (UC) and Crohn's disease (CD), based on histological appearance and anatomical distribution. However, an increasing body of data supports the concept that IBD is an umbrella diagnosis encompassing a variety of disorders with distinct genetic, microbial, and environmental determinants that cluster either into a UC or CD phenotype. The shared common pathway is uncontrolled intestinal inflammation. A key element in the pathogenesis of intestinal inflammation in both UC and CD is increased leukocyte recruitment from the circulation, and this provides a potential target for pharmaceutical inhibition. In this article we review the current understanding of the molecules that determine leukocyte trafficking to the gut and highlight opportunities where their inhibition could be exploited to treat IBD.(Inflamm Bowel Dis 2008).

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Complex regulation of CCR9 at multiple discrete stages of T cell development

Cited by 61 publications

References 27 publications

Impaired Accumulation of Antigen-Specific CD8 Lymphocytes in Chemokine CCL25-Deficient Intestinal Epithelium and Lamina Propria

Impaired Accumulation of Antigen-Specific CD8 Lymphocytes in Chemokine CCL25-Deficient Intestinal Epithelium and Lamina Propria

The Role of Transferrin in Actinide(IV) Uptake: Comparison with Iron(III)

Lymphocyte homing and its role in the pathogenesis of IBD

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