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In vivo expression of natural killer cell inhibitory receptors by human melanoma-specific cytolytic T lymphocytes. J. Exp. Med. 190: 775",{"doi":606},"10.1084\u002Fjem.190.6.775",{"id":24,"text":608,"url":24,"identifiers":609},"De Maria, A.,  A. Ferraris,  M. Guastella,  S. Pilia,  C. Cantoni,  L. Polero,  M. C. Mingari,  D. Bassetti,  A. S. Fauci,  L. Moretta.  1997. Expression of HLA class I-specific inhibitory natural killer cell receptors in HIV-specific cytolytic T lymphocytes: impairment of specific cytolytic functions. Proc. Natl. Acad. Sci. USA 94: 10285",{"doi":610},"10.1073\u002Fpnas.94.19.10285",{"id":24,"text":612,"url":24,"identifiers":613},"Zajac, A. J.,  R. E. Vance,  W. Held,  D. J. Sourdive,  J. D. Altman,  D. H. Raulet,  R. Ahmed.  1999. Impaired anti-viral T cell responses due to expression of the Ly49A inhibitory receptor. J. Immunol. 163: 5526",{"doi":614},"10.4049\u002Fjimmunol.163.10.5526",false,{"id":617,"createTime":618,"updateTime":619,"relativeEntities":620,"slug":621,"properties":622,"entityType":295,"verifyStatus":296,"verifyTime":618,"verifyNote":297,"languages":637,"translateLanguages":24,"viewCount":25,"primaryUrl":638,"fullTextUrl":24,"authors":639,"publicationType":423,"publisherRelationship":856,"citationCount":25,"citationInfo":911,"publishDate":914,"publishYear":912,"citationAnalyzeStatus":915,"lastCitationAnalyze":619,"indexDatabases":916,"openAccess":24,"references":917,"isForceReanalyzing":615},"7a6e8d75-663a-4fe1-8053-274c2a158592","2024-10-15T23:08:03.077+00:00","2026-07-30T00:19:39.718+00:00",[],"Cytokine-control-of-parasite-specific-anergy-in-human-urinary-schistosomiasis-IL-10-modulates-lymphocyte-reactivity-",{"mag":623,"gsPaper":625,"openalex":627,"abstract":629,"title":631,"pm":633,"doi":635},{"VOID":624},"2106459612",{"VOID":626},"[\"7782851993250575498\"]",{"VOID":628},"W2106459612",{"EN":630},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:p>Humans chronically infected with schistosomiasis usually have impaired parasite Ag-specific lymphocyte proliferation and IFN-gamma production that may facilitate persistence of the parasite while producing little clinical disease. The mechanisms that contribute to the immunologic hyporesponsiveness in these patients remain undefined. IL-10 has been shown to exert an inhibitory effect on cell-mediated immunity. To determine whether endogenous IL-10 has a role in regulating parasite-specific anergy in schistosomiasis, neutralizing anti-IL-10 added to PBMC from Schistosoma haematobium patients' enhanced adult worm (SWAP)- or egg Ag (SEA)-driven lymphocyte proliferation and\u002For IFN-gamma production by 2- to &amp;gt;100-fold in 32 of 38 subjects. In contrast, anti-IL-10 failed to significantly augment the mycobacterial Ag, purified protein derivative (PPD)-driven lymphocyte proliferation, or IFN-gamma production in 9 or 10 of 14 individuals, respectively. SWAP or SEA triggered IL-10 release from PBMC of both patients and healthy individuals; however, CD4+ cells were a significant source of IL-10 only in infected subjects. PPD relative to SWAP induced fivefold less IL-10 release by CD4+ cells (p &amp;lt; 0.01). A possible mechanism whereby IL-10 suppressed Ag-specific T cell responses was demonstrated by the ability of SWAP and not PPD to suppress B7 expression on PBMC. Anti-IL-10 completely inhibited the parasite Ag-induced down-regulation of B7 expression. These studies indicate that IL-10 contributes to parasite Ag-induced T cell hyporesponsiveness observed in patients with chronic schistosomiasis hematobia.\u003C\u002Fjats:p>",{"EN":632},"Cytokine control of parasite-specific anergy in human urinary schistosomiasis. 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T cell receptor genes in a series of class I major histocompatibility complex-restricted cytotoxic T cell clones specific for a Plasmodium berghei nonapeptide: implications for T cell allelic exclusion and antigen-specific repertoire. J. Exp. Med. 174: 1371",{"doi":1076},"10.1084\u002Fjem.174.6.1371",{"id":24,"text":1078,"url":24,"identifiers":1079},"Kuida, K.,  M. Furutani-Seiki,  T. Saito,  H. Kishimoto,  K. Sano,  T. Tada.  1991. Post-translational attainment of allelic exclusion of the T cell receptor α chain in a T cell clone. Int. Immunol. 3: 75",{"doi":1080},"10.1093\u002Fintimm\u002F3.1.75",{"id":24,"text":1082,"url":24,"identifiers":1083},"Couez, D.,  M. Malissen,  M. Buferne,  A.-M. Schmitt-Verhulst,  B. Malissen.  1991. Each of the two productive T cell receptor α-gene rearrangements found in both the A10 and BM 3.3 T cell clones give rise to an α chain which can contribute to the constitution of a surface-expressed αβ dimer. Int. Immunol. 3: 719",{"doi":1084},"10.1093\u002Fintimm\u002F3.7.719",{"id":24,"text":1086,"url":24,"identifiers":1087},"Kearse, K. P.,  J. L. Roberts,  T. I. Munitz,  D. L. Wiest,  T. Nakayama,  A. Singer.  1994. Developmental regulation of αβ T cell antigen receptor expression results from differential stability of nascent TCRα proteins within the endoplasmic reticulum of immature and mature T cells. EMBO J. 13: 4504",{"doi":1088},"10.1002\u002Fj.1460-2075.1994.tb06772.x",{"id":24,"text":1090,"url":24,"identifiers":1091},"Kearse, K. P.,  Y. Takahama,  J. A. Punt,  S. O. Sharrow,  A. Singer.  1995. Early molecular events induced by T cell receptor (TCR) signaling in immature CD4+CD8+ thymocytes: increased synthesis of TCR-α protein is an early response to TCR signaling that compensates for TCR-α instability, improves TCR assembly, and parallels other indicators of positive selection. J. Exp. Med. 181: 193",{"doi":1092},"10.1084\u002Fjem.181.1.193",{"id":24,"text":1094,"url":24,"identifiers":1095},"Kosugi, A.,  A. M. Weissman,  M. Ogata,  T. Hamaoka,  H. Fujiwara.  1992. Instability of assembled T-cell receptor complex that is associated with rapid degradation of ζ chains in immature CD4+CD8+ thymocytes. Proc. Natl. Acad. Sci. USA 89: 9494",{"doi":1096},"10.1073\u002Fpnas.89.20.9494",{"id":24,"text":1098,"url":24,"identifiers":1099},"Havran, W. L.,  M. Poenie,  J. Kimura,  R. Tsien,  A. Weiss,  J. P. Allison.  1987. Expression and function of the CD3-antigen receptor on murine CD4+8+ thymocytes. Nature 330: 170",{"doi":1100},"10.1038\u002F330170a0",{"id":24,"text":1102,"url":24,"identifiers":1103},"Crispe, I. N.,  R. P. Shimonkevitz,  L. A. Husmann,  J. Kimura,  J. P. Allison.  1987. Expression of T cell antigen receptor β-chains on subsets of mouse thymocytes: analysis by three-color flow cytometry. J. Immunol. 139: 3585",{"doi":1104},"10.4049\u002Fjimmunol.139.11.3585",{"id":24,"text":1106,"url":24,"identifiers":1107},"Padovan, E.,  G. Casorati,  P. Dellabona,  S. Meyer,  M. Brockhaus,  A. Lanzavecchia.  1993. Expression of two T cell receptor α chains: dual receptor T cells. Science 262: 422",{"doi":1108},"10.1126\u002Fscience.8211163",{"id":24,"text":1110,"url":24,"identifiers":1111},"Heath, W. R.,  F. R. Carbone,  P. Bertolino,  J. Kelly,  S. Cose,  J. F. A. P. Miller.  1995. Expression of two T cell receptor α chains on the surface of normal murine T cells. Eur. J. Immunol. 25: 1617",{"doi":1112},"10.1002\u002Feji.1830250622",{"id":24,"text":1114,"url":24,"identifiers":1115},"Elliott, J. I.,  D. M. Altmann.  1995. Dual T cell receptor α chain T cells in autoimmunity. J. Exp. Med. 182: 953",{"doi":1116},"10.1084\u002Fjem.182.4.953",{"id":24,"text":1118,"url":24,"identifiers":1119},"Mombaerts, P.,  A. R. Clarke,  M. A. Rudnicki,  J. Iacomini,  S. Itohara,  J. Lafaille,  L. Wang,  Y. Ichikawa,  R. Jaenisch,  M. L. Hooper,  S. Tonegawa.  1992. Mutations in T cell receptor genes α and β block thymocyte development at different stages. Nature 360: 225",{"doi":1120},"10.1038\u002F360225a0",{"id":24,"text":1122,"url":24,"identifiers":1123},"Pircher, H.,  N. Rebaï,  M. Groettrup,  C. Grégoire,  D. E. Speiser,  M. P. Happ,  E. Palmer,  R. M. Zinkernagel,  H. Hengartner,  B. Malissen.  1992. Preferential positive selection of Vα2+CD8+ T cells in mouse strains expressing both H-2k and T cell receptor Vαa haplotypes: determination with a Vα2-specific monoclonal antibody. Eur. J. Immunol. 22: 399",{"doi":1124},"10.1002\u002Feji.1830220217",{"id":24,"text":1126,"url":24,"identifiers":1127},"Utsunomiya, Y.,  J. Bill,  E. Palmer,  K. Gollob,  Y. Takagaki,  O. Kanagawa.  1989. Analysis of a monoclonal rat antibody directed to the α-chain variable region (Vα3) of the mouse T cell antigen receptor. J. Immunol. 143: 2602",{"doi":1128},"10.4049\u002Fjimmunol.143.8.2602",{"id":24,"text":1130,"url":24,"identifiers":1131},"Necker, A.,  N. Rebaï,  M. Matthes,  E. Jouvin-Marche,  P.-A. Cazenave,  P. Swarnworawong,  E. Palmer,  H. R. MacDonald,  B. Malissen.  1991. Monoclonal antibodies raised against engineered soluble mouse T cell receptors and specific for Vα8-, Vβ2-, or Vβ10-bearing T cells. Eur. J. Immunol. 21: 3035",{"doi":1132},"10.1002\u002Feji.1830211220",{"id":24,"text":1134,"url":24,"identifiers":1135},"Jameson, S. C.,  P. B. Nakajima,  J. L. Brooks,  W. Heath,  O. Kanagawa,  N. R. J. Gascoigne.  1991. The T cell receptor Vα11 gene family: analysis of allelic sequence polymorphism and demonstration of Jα region-dependent recognition by allele-specific antibodies. J. Immunol. 147: 3185",{"doi":1136},"10.4049\u002Fjimmunol.147.9.3185",{"id":24,"text":1138,"url":24,"identifiers":1139},"Kubo, R. T.,  W. Born,  J. W. Kappler,  P. Marrack,  M. Pigeon.  1989. Characterization of a monoclonal antibody which detects all murine αβ T cell receptors. J. Immunol. 142: 2736",{"doi":1140},"10.4049\u002Fjimmunol.142.8.2736",{"id":24,"text":1142,"url":24,"identifiers":1143},"Gascoigne, N. R. J..  1990. Transport and secretion of truncated T cell receptor β-chain occurs in the absence of association with CD3. J. Biol. Chem. 265: 9296",{"doi":1144},"10.1016\u002FS0021-9258(19)38847-7",{"id":24,"text":1146,"url":24,"identifiers":1147},"Alam, S. M.,  P. Whitford,  W. Cushley,  W. D. George,  A. M. Campbell.  1992. Aneuploid subpopulations in tumour-invaded lymph nodes from breast cancer patients. Eur. J. Cancer 28: 357",{"doi":1148},"10.1016\u002FS0959-8049(05)80053-X",{"id":24,"text":1150,"url":24,"identifiers":1151},"Klausner, R. D.,  J. Lippincott-Schwartz,  J. S. Bonifacino.  1990. The T cell antigen receptor: insights into organelle biology. Annu. Rev. 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Although poorly defined, mesenchymal stem cells (MSC) appear useful for applications in repair medicine. Despite the low frequency of MSC, they are relatively easy to expand. The expression of MHC class II on MSC, however, could deter their use in repair medicine, since these molecules could stimulate an allogeneic host response. This study sought to compare the immune stimulatory and suppressive effects of MSC. Primary human MSC were cultured from bone marrow aspirates and then passaged at least three times before use in assays. Morphologically, MSC were symmetrical; were SH2+, MHC class II+, CD45−, CD44+, CD31−, CD14−, proly-4-hydroxylase−; and showed normal karyotype patterns and elevated telomerase activities. MSC elicited significant stimulatory responses when cocultured with allogeneic PBMC. Despite the production of different types of growth factors, allogeneic effects of MSC could not be explained by the production of these growth factors. One-way MLR reactions were significantly blunted by third-party MSC. Similar suppression was not observed for responses to three different recall Ags. Based on these functional differences by MSC in responses to allo- and recall Ags, we examined whether MSC could exert veto-like functions. We showed that MSC could blunt the cytotoxic effects of allogeneic-induced effectors to mitogen-activated targets. 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I..  1995. Developmental biology of hematopoiesis. Blood 86:2876.",{"doi":1355},"10.1182\u002Fblood.V86.8.2876.bloodjournal8682876",{"id":24,"text":1357,"url":24,"identifiers":1358},"Deans, R. J.,  A. B. Moseley.  2000. Mesenchymal stem cells: biology and potential clinical uses. Exp Hematol. 28:875.",{"doi":1359},"10.1016\u002FS0301-472X(00)00482-3",{"id":24,"text":1361,"url":24,"identifiers":1362},"Jiang, Y.,  B. N. Jahagirdar,  R. L. Reinhardt,  R. E. Schwartz,  C. D. Keene,  R. Ortiz-Gonzalez,  M. Reyes,  T. Lenvik,  T. Lund,  M. Blackstad, et al 2002. Pluripotency of mesenchymal stem cells derived from adult marrow. Nature 418:41.",{"doi":1363},"10.1038\u002Fnature00870",{"id":24,"text":1365,"url":24,"identifiers":1366},"Arai, F.,  O. Ohneda,  T. Miyamoto,  X. Q. Zhang,  T. Suda.  2002. Mesenchymal stem cells in perichondrium express activated leukocyte cell adhesion molecule and participate in bone marrow formation. J. Exp. 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MHC alloantigens elicit secondary, but not primary, indirect in vitro proliferative responses. J. Immunol. 169:3613.",{"doi":1523},"10.4049\u002Fjimmunol.169.7.3613",{"id":1525,"createTime":1526,"updateTime":1527,"relativeEntities":1528,"slug":1529,"properties":1530,"entityType":295,"verifyStatus":296,"verifyTime":1545,"verifyNote":297,"languages":1546,"translateLanguages":24,"viewCount":25,"primaryUrl":1547,"fullTextUrl":24,"authors":1548,"publicationType":423,"publisherRelationship":1647,"citationCount":1701,"citationInfo":1702,"publishDate":1705,"publishYear":1703,"citationAnalyzeStatus":23,"lastCitationAnalyze":1706,"indexDatabases":1707,"openAccess":24,"references":1708,"isForceReanalyzing":615},"79ce4775-e3b6-4886-815c-0d076fc67aca","2024-09-02T11:40:00.146+00:00","2026-07-22T21:51:44.249+00:00",[],"Deregulated-Bcl-2-gene-expression-selectively-prolongs-survival-of-growth-factor-deprived-hemopoietic-cell-lines-",{"mag":1531,"gsPaper":1533,"openalex":1535,"abstract":1537,"title":1539,"pm":1541,"doi":1543},{"VOID":1532},"1554380543",{"VOID":1534},"[\"13945499406794198649\"]",{"VOID":1536},"W1554380543",{"EN":1538},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:p>The t(14;18) of human follicular B cell lymphoma translocates the Bcl-2 gene into the Ig H chain locus and markedly deregulates Bcl-2 expression. We sought to determine if Bcl-2 could be directly implicated in a growth-factor pathway. Consequently, we introduced a retrovirus containing the murine Bcl-2 gene (N2-M-Bcl-2) or the parental retrovirus (N2) into a series of factor-dependent hemopoietic cell lines. Overexpressed Bcl-2 resulted in no long term IL-2, IL-3, or IL-6 independent clones, indicating that Bcl-2 could not spare the need for a specific ligand-receptor interaction. However, Bcl-2 did extend the short term survival of IL-3-dependent cell lines after factor deprivation. Although viable, IL-3-deprived pro B lymphocytes (FL5.12) bearing N2-M-Bcl-2 were in Go, and deregulated Bcl-2 did not obviously influence cell-cycle progression. Bcl-2 predominant effects were to delay the onset of cell death and to modestly augment viable cell growth in the first 48 h after IL-3 deprivation. This death sparing was associated with increased levels of Bcl-2 RNA and protein in factor-deprived cells possessing N2-M-Bcl-2. This result was not restricted to prolymphocytes because an IL-3-dependent mast cell line (32D) as well as a promyeloid line (FDC-P1) demonstrated the same response to Bcl-2. Moreover, the effect was not limited to the IL-3\u002FIL-3R signal transduction pathway in that promyeloid cells maintained in granulocyte-macrophage-CSF or IL-4 displayed a similar response. Yet, Bcl-2-enhanced cell survival was not universal as an IL-2-dependent T cell line, and an IL-6-dependent myeloma line demonstrated no consistent effect upon IL withdrawal. Thus, Bcl-2 appears to interfere with cell death but in a cell type and\u002For factor-restricted fashion.\u003C\u002Fjats:p>",{"EN":1540},"Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines.",{"VOID":1542},"2184193",{"VOID":1544},"10.4049\u002Fjimmunol.144.9.3602","2024-09-02T11:40:00.145+00:00",[299],"https:\u002F\u002Fjournals.aai.org\u002Fjimmunol\u002Farticle\u002F144\u002F9\u002F3602\u002F110574\u002FDeregulated-Bcl-2-gene-expression-selectively",[1549,1568,1585,1600,1617,1632],{"id":1550,"sortIndex":25,"researcher":24,"roles":1551,"affiliations":1552,"properties":1561,"displayName":1565,"givenName":24,"familyName":24},"82ecb859-c1e2-40d2-910e-3ff06452eb0b",[],[1553],{"id":1554,"sortIndex":25,"affiliation":1555,"properties":24},"076d90e0-1e37-4c48-8d4a-9436c0769944",{"id":1554,"createTime":24,"updateTime":24,"relativeEntities":1556,"slug":24,"properties":1557,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1560,"statistic":24},[],{"title":1558},{"EN":1559},"Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110.",[],{"orcid":1562,"title":1564,"openalex":1566},{"VOID":1563},"https:\u002F\u002Forcid.org\u002F0000-0002-6529-2695",{"EN":1565},"Gabriel Núñez",{"VOID":1567},"A5040117830",{"id":1569,"sortIndex":110,"researcher":24,"roles":1570,"affiliations":1571,"properties":1578,"displayName":1582,"givenName":24,"familyName":24},"06505476-42e2-43dd-82fe-bca4ee4220f4",[],[1572],{"id":1554,"sortIndex":25,"affiliation":1573,"properties":24},{"id":1554,"createTime":24,"updateTime":24,"relativeEntities":1574,"slug":24,"properties":1575,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1577,"statistic":24},[],{"title":1576},{"EN":1559},[],{"orcid":1579,"title":1581,"openalex":1583},{"VOID":1580},"https:\u002F\u002Forcid.org\u002F0000-0003-1297-2758",{"EN":1582},"Leslie London",{"VOID":1584},"A5047948007",{"id":1586,"sortIndex":109,"researcher":24,"roles":1587,"affiliations":1588,"properties":1595,"displayName":1597,"givenName":24,"familyName":24},"1e9ef9a0-7c4c-4cee-96af-71623bdc3f37",[],[1589],{"id":1554,"sortIndex":25,"affiliation":1590,"properties":24},{"id":1554,"createTime":24,"updateTime":24,"relativeEntities":1591,"slug":24,"properties":1592,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1594,"statistic":24},[],{"title":1593},{"EN":1559},[],{"title":1596,"openalex":1598},{"EN":1597},"David M. Hockenbery",{"VOID":1599},"A5016626619",{"id":1601,"sortIndex":111,"researcher":24,"roles":1602,"affiliations":1603,"properties":1610,"displayName":1614,"givenName":24,"familyName":24},"1e96cb05-38cc-47ff-86e2-3f772ae4a565",[],[1604],{"id":1554,"sortIndex":25,"affiliation":1605,"properties":24},{"id":1554,"createTime":24,"updateTime":24,"relativeEntities":1606,"slug":24,"properties":1607,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1609,"statistic":24},[],{"title":1608},{"EN":1559},[],{"orcid":1611,"title":1613,"openalex":1615},{"VOID":1612},"https:\u002F\u002Forcid.org\u002F0000-0003-3455-0716",{"EN":1614},"Martha A. 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Bulfone-Paus. 2004. Reverse signaling through membrane-bound interleukin-15. J. Biol. Chem. 279: 42192-42201.",{"doi":2319},"10.1074\u002Fjbc.M403182200",{"id":24,"text":2321,"url":24,"identifiers":2322},"Rubinstein, M. P., M. Kovar, J. F. Purton, J. H. Cho, O. Boyman, C. D. Surh, J. Sprent. 2006. Converting IL-15 to a superagonist by binding to soluble IL-15Rα. Proc. Natl. Acad. Sci. USA 103: 9166-9171.",{"doi":2323},"10.1073\u002Fpnas.0600240103",{"id":2325,"createTime":2326,"updateTime":2327,"relativeEntities":2328,"slug":2329,"properties":2330,"entityType":295,"verifyStatus":296,"verifyTime":2345,"verifyNote":297,"languages":2346,"translateLanguages":24,"viewCount":25,"primaryUrl":2347,"fullTextUrl":24,"authors":2348,"publicationType":423,"publisherRelationship":2596,"citationCount":113,"citationInfo":2651,"publishDate":2654,"publishYear":2652,"citationAnalyzeStatus":23,"lastCitationAnalyze":2655,"indexDatabases":2656,"openAccess":24,"references":2657,"isForceReanalyzing":615},"a73f2d08-e660-4818-815f-3fcf253a10a1","2024-12-12T07:19:38.755+00:00","2026-07-21T03:34:04.993+00:00",[],"Expansion-of-Group-2-Innate-Lymphoid-Cells-in-Patients-with-End-Stage-Renal-Disease-and-Their-Clinical-Significance",{"mag":2331,"gsPaper":2333,"openalex":2335,"abstract":2337,"title":2339,"pm":2341,"doi":2343},{"VOID":2332},"3027198349",{"VOID":2334},"[\"4951921863675510307\"]",{"VOID":2336},"W3027198349",{"EN":2338},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:p>Group 2 innate lymphoid cells (ILC2s) play an important role in the control of tissue inflammation and homeostasis. However, the role of ILC2s in patients with end-stage renal disease (ESRD) has never been illustrated. In this study, we investigated ILC2s in ESRD patients and their clinical significance. Results showed that the frequencies and absolute numbers of ILC2s, not group 1 innate lymphoid cells or innate lymphoid cell precursors, were significantly elevated in the peripheral blood of ESRD patients when compared with those from healthy donor controls. Moreover, ILC2s from ESRD patients displayed enhanced type 2 cytokine production and cell proliferation. Plasma from ESRD patients significantly increased ILC2 levels and enhanced their effector function after in vitro treatment. The expression of phosphorylation of STAT5 in ILC2s, as well as the amounts of IL-2 in plasma, were increased in ESRD patients when compared with those from healthy donors. Clinically, ESRD patients with higher ILC2 frequencies displayed lower incidence of infectious complications during a mean of 21 month follow-up study. The proportions of ILC2s were negatively correlated with the prognostic biomarkers of chronic kidney disease, including serum parathyroid hormone, creatinine, and phosphorus, whereas they were positively correlated with serum calcium. These observations indicate that ILC2s may play a protective role in ESRD.\u003C\u002Fjats:p>",{"EN":2340},"Expansion of Group 2 Innate Lymphoid Cells in Patients with End-Stage Renal Disease and Their Clinical Significance",{"VOID":2342},"32444391",{"VOID":2344},"10.4049\u002Fjimmunol.1901095","2024-12-12T07:19:38.754+00:00",[299],"https:\u002F\u002Fjournals.aai.org\u002Fjimmunol\u002Farticle\u002F205\u002F1\u002F36\u002F110127\u002FExpansion-of-Group-2-Innate-Lymphoid-Cells-in",[2349,2382,2411,2430,2459,2478,2495,2520,2539,2556,2573],{"id":2350,"sortIndex":25,"researcher":24,"roles":2351,"affiliations":2352,"properties":2377,"displayName":2379,"givenName":24,"familyName":24},"698ed590-3eb9-493a-9540-840c5a56d01f",[],[2353,2361,2369],{"id":2354,"sortIndex":25,"affiliation":2355,"properties":24},"be974742-8a47-466e-a8c7-b88be8ce3a17",{"id":2354,"createTime":24,"updateTime":24,"relativeEntities":2356,"slug":24,"properties":2357,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2360,"statistic":24},[],{"title":2358},{"EN":2359},"*Joint Program in Immunology, Department of Internal Medicine, Affiliated Guangzhou Women and Children’s Medical Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510623, China;",[],{"id":2362,"sortIndex":110,"affiliation":2363,"properties":24},"4853df5b-0eda-4068-9ec1-9d2ca1375b55",{"id":2362,"createTime":24,"updateTime":24,"relativeEntities":2364,"slug":24,"properties":2365,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2368,"statistic":24},[],{"title":2366},{"VI":2367},"Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China",[],{"id":2370,"sortIndex":109,"affiliation":2371,"properties":24},"088d04a8-2666-48d0-8d8b-fdf88e32b129",{"id":2370,"createTime":24,"updateTime":24,"relativeEntities":2372,"slug":24,"properties":2373,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2376,"statistic":24},[],{"title":2374},{"VI":2375},"Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China",[],{"title":2378,"openalex":2380},{"EN":2379},"Gao-Yu 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Renal Physiol., 318, F475, 10.1152\u002Fajprenal.00407.2019",{"doi":2920},"10.1152\u002Fajprenal.00407.2019",{"id":2922,"createTime":2923,"updateTime":2924,"relativeEntities":2925,"slug":2926,"properties":2927,"entityType":295,"verifyStatus":296,"verifyTime":2941,"verifyNote":297,"languages":2942,"translateLanguages":24,"viewCount":25,"primaryUrl":2943,"fullTextUrl":24,"authors":2944,"publicationType":423,"publisherRelationship":3045,"citationCount":3099,"citationInfo":3100,"publishDate":3103,"publishYear":3101,"citationAnalyzeStatus":1855,"lastCitationAnalyze":3104,"indexDatabases":3105,"openAccess":24,"references":3106,"isForceReanalyzing":615},"addf0a11-ba9b-417f-815f-a17380c071bc","2024-10-07T09:16:00.420+00:00","2026-07-20T20:42:31.773+00:00",[],"Activation-of-the-Lectin-Complement-Pathway-by-H-Ficolin-Hakata-Antigen-",{"mag":2928,"gsPaper":2930,"openalex":2931,"abstract":2933,"title":2935,"pm":2937,"doi":2939},{"VOID":2929},"1923930491",{"VOID":1719},{"VOID":2932},"W1923930491",{"EN":2934},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Ficolins are a group of proteins which consist of a collagen-like domain and a fibrinogen-like domain. In human serum, there are two types of ficolins named L-ficolin\u002FP35 and H-ficolin (Hakata Ag), both of which have lectin activity. We recently demonstrated that L-ficolin\u002FP35 is associated with mannose-binding lectin (MBL)-associated serine proteases (MASP) 1 and 2 and small MBL-associated protein (sMAP), and that the complex activates the lectin pathway. In this study, we report the characterization of H-ficolin in terms of its ability to activate complement. Western blotting analysis showed the presence of MASP-1, MASP-2, MASP-3, and sMAP in H-ficolin preparations isolated from Cohn Fraction III. The MASPs in the preparations had proteolytic activities against C4, C2, and C3 in the fluid phase. When H-ficolin preparations were bound to anti-H-ficolin Ab which had been coated on ELISA plates, they activated C4, although no C4 activation was noted when anti-MBL and anti-L-ficolin\u002FP35 were used. H-ficolin binds to PSA, a polysaccharide produced by Aerococcus viridans. C4 was activated by H-ficolin preparations bound to PSA which had been coated on ELISA plates. These results indicate that H-ficolin is a second ficolin which is associated with MASPs and sMAP, and which activates the lectin pathway.\u003C\u002Fjats:p>",{"EN":2936},"Activation of the Lectin Complement Pathway by H-Ficolin (Hakata 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Japan",[],{"orcid":2958,"title":2960,"openalex":2962},{"VOID":2959},"https:\u002F\u002Forcid.org\u002F0000-0002-0351-0562",{"EN":2961},"Misao Matsushita",{"VOID":2963},"A5009306852",{"id":2965,"sortIndex":110,"researcher":24,"roles":2966,"affiliations":2967,"properties":2974,"displayName":2976,"givenName":24,"familyName":24},"24f68d60-7a47-43f1-b211-4c28cb127755",[],[2968],{"id":2950,"sortIndex":25,"affiliation":2969,"properties":24},{"id":2950,"createTime":24,"updateTime":24,"relativeEntities":2970,"slug":24,"properties":2971,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2973,"statistic":24},[],{"title":2972},{"VI":2955},[],{"title":2975,"openalex":2977},{"EN":2976},"Mikio 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Hamasaki",{"VOID":2995},"A5048838957",{"id":2997,"sortIndex":111,"researcher":24,"roles":2998,"affiliations":2999,"properties":3008,"displayName":3010,"givenName":24,"familyName":24},"e3ee6be3-cd31-4bb3-b504-7e491053f384",[],[3000],{"id":3001,"sortIndex":25,"affiliation":3002,"properties":24},"51f05e25-d0a3-479a-b918-0fbf4c807c43",{"id":3001,"createTime":24,"updateTime":24,"relativeEntities":3003,"slug":24,"properties":3004,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3007,"statistic":24},[],{"title":3005},{"EN":3006},"‡Fukuoka Red Cross Blood Center, Chikushino, Japan",[],{"title":3009,"openalex":3011},{"EN":3010},"Mitsushi 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A truncated form of mannose-binding lectin-associated serine protease (MASP)-2 expressed by alternative polyadenylation is a component of the lectin complement pathway. Int. Immunol. 11: 859",{"doi":3209},"10.1093\u002Fintimm\u002F11.5.859",{"id":24,"text":3211,"url":24,"identifiers":3212},"Stover, C. D., S. Thiel, M. Thelen, N. J. Lynch, T. Vorup-Jensen, J. C. Jensenius, W. J. Schwaeble. 1999. Two constituents of the initiation complex of the mannan-binding lectin activation pathway of the complement are encoded by a single structural gene. J. Immunol. 162: 3481",{"doi":3213},"10.4049\u002Fjimmunol.162.6.3481",{"id":24,"text":3215,"url":24,"identifiers":3216},"Matsushita, M., S. Thiel, J. C. Jensenius, I. Terai, T. Fujita. 2000. Proteolytic activities of two types of mannose-binding lectin-associated serine protease. J. Immunol. 165: 2637",{"doi":3217},"10.4049\u002Fjimmunol.165.5.2637",{"id":24,"text":3219,"url":24,"identifiers":3220},"Vorup-Jensen, T., S. V. Petersen, A. G. 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