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CpG had an adjuvant effect on IgA production in genital tract washes when administered intranasally but only affected IgA production in faeces samples when administered intraperitoneally. In addition, IgA was also detected in mucosal tissues from the lung and intestine, while CpG induced an increased level of IgA in the intestine. Most importantly, neutralization antibodies were detected in sera after i.p. and intranasal (i.n.) immunizations. Secretions in genital tract washes from the i.n. group also showed neutralization activity. Furthermore, VLPs that were administered intraperitoneally elicited cellular immune responses as demonstrated by enzyme‐linked immunospot (ELISPOT) assay analyses. 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PRL itself can also generate LAK activity. Here we show that its local production occurs during, and is necessary for, LAK development. IL‐2‐stimulated peripheral blood mononuclear cells (PBMC) and purified NK cells were exposed to anti‐human (h)PRL antiserum, and residual LAK activity was measured on day 7 against the promyelocytic leukaemia cell line HL‐60. Inhibition of LAK activity was much more evident in PBMC compared with NK cell cultures (47% decrease, \u003Cjats:italic>P\u003C\u002Fjats:italic>=0.013 and 18.5% decrease, \u003Cjats:italic>P\u003C\u002Fjats:italic>=0.048, respectively). Up‐modulation of a \u003Cjats:sup>32\u003C\u002Fjats:sup>S‐methionine‐labelled 27000MW protein was detected in the lysates and supernatants of IL‐2‐stimulated PBMC immunoprecipitated with an anti‐PRL antiserum. 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In particular, the constitutive natural killer (NK) and the lymphokine‐activated killer (LAK) cytotoxicity of CD56\u003Cjats:sup>+\u003C\u002Fjats:sup> CD16\u003Cjats:sup>+\u003C\u002Fjats:sup> cells is increased by its physiological to supraphysiological concentrations. As PRL has been shown to up‐regulate the production of interferon‐γ (IFN‐γ) by peripheral blood mononuclear cells, we studied its effect on IFN‐γ production by NK cells as a possible mechanism of autocrine activation of cytotoxicity. Released and intracellular IFN‐γ, as well as IFN‐γ mRNA expression, were increased by pituitary and recombinant human PRL, which stimulated optimal NK and LAK cytotoxicity. Treatment with blocking anti‐IFN‐γ monoclonal antibody (mAb) selectively affected PRL‐increased killing of K562 targets, demonstrating that PRL‐mediated enhancement of spontaneous cytotoxicity depends, at least in part, on up‐regulation of IFN‐γ.\u003C\u002Fjats:p>",{"EN":802},"Up‐modulation of interferon‐γ mediates the enhancement of spontanous cytotoxicity in prolactin‐activated natural killer cells",{"VOID":804},"10583598",{"VOID":806},"10.1046\u002Fj.1365-2567.1999.00893.x","2024-09-05T23:41:51.606+00:00","Author affiliation is blank",[192],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1046\u002Fj.1365-2567.1999.00893.x",[812,821,830,848,855],{"id":813,"sortIndex":113,"researcher":23,"roles":814,"affiliations":815,"properties":816},"b9e70f06-ca06-45f0-b86e-86ddb7f574ac",[],[],{"openalex":817,"title":819},{"VOID":818},"A5001203453",{"EN":820},"B Forno",{"id":822,"sortIndex":117,"researcher":23,"roles":823,"affiliations":824,"properties":825},"8a04bc78-d471-4199-a805-1303d4e59835",[],[],{"openalex":826,"title":828},{"VOID":827},"A5022621924",{"EN":829},"A Biglino",{"id":831,"sortIndex":24,"researcher":23,"roles":832,"affiliations":833,"properties":845},"cb919e01-3c3c-48bd-bb21-b510be23b238",[],[834],{"id":835,"sortIndex":24,"affiliation":836,"properties":23},"f0da4dba-eecd-4ba8-998a-dcb60a5e08db",{"id":837,"createTime":838,"updateTime":839,"relativeEntities":840,"slug":841,"properties":842,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"901af635-842a-4eea-bd1f-2a8c58fea05a","2023-12-11T18:51:11.206+00:00","2025-01-26T10:39:42.762+00:00",[],"Department-of-Internal-Medicine-University-of-Turin-Italy",{"title":843},{"VI":844},"Department of Internal Medicine, University of Turin, Italy",{"openalex":846,"title":847},{"VOID":635},{"EN":637},{"id":849,"sortIndex":118,"researcher":23,"roles":850,"affiliations":851,"properties":852},"0f6ad101-5861-40c7-9912-2de2e6bb1471",[],[],{"openalex":853,"title":854},{"VOID":724},{"EN":726},{"id":856,"sortIndex":119,"researcher":23,"roles":857,"affiliations":858,"properties":859},"30fb9cf8-73a2-4844-85d5-c991c5a62b61",[],[],{"openalex":860,"title":861},{"VOID":684},{"EN":862},"M. 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lymphocytes: antagonism of prolactin binding by cyclosporin., J Immunol, 134, 3027, 10.4049\u002Fjimmunol.134.5.3027",{"doi":969},"10.4049\u002Fjimmunol.134.5.3027",{"id":23,"text":971,"url":23,"identifiers":972},"10.1016\u002F0889-1591(88)90001-3",{"doi":971},{"id":23,"text":974,"url":23,"identifiers":975},"10.3181\u002F00379727-205-43683",{"doi":974},{"id":23,"text":977,"url":23,"identifiers":978},"10.1146\u002Fannurev.immunol.16.1.359",{"doi":977},{"id":23,"text":980,"url":23,"identifiers":981},"10.1007\u002F978-3-642-46859-9_2",{"doi":980},{"id":23,"text":983,"url":23,"identifiers":984},"10.1016\u002FS0952-7915(98)80163-5",{"doi":983},{"id":23,"text":986,"url":23,"identifiers":987},"Cosman D., 1997, Interleukin 15., Biochem Soc Trans, 25, 371, 10.1042\u002Fbst0250371",{"doi":988},"10.1042\u002Fbst0250371",{"id":23,"text":990,"url":23,"identifiers":991},"10.1084\u002Fjem.188.11.2067",{"doi":990},{"id":23,"text":993,"url":23,"identifiers":994},"Berczi I., 1993, Prolactin, pregnancy 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In addition, these cells express increased levels of inhibitory receptors and display defective Akt(ser\u003Cjats:sup>473\u003C\u002Fjats:sup>) phosphorylation following activation. It is not known whether signalling via programmed death 1 (PD‐1) contributes to any of the attenuated differentiation‐related functional changes in CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells. To address this we blocked PD‐1 signalling during T‐cell receptor (TCR) activation using antibodies against PD‐1 ligand 1 (PDL1) and PDL2. This resulted in a significant enhancement of Akt(ser\u003Cjats:sup>473\u003C\u002Fjats:sup>) phosphorylation and TCR‐induced proliferative activity of highly differentiated CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> CD28\u003Cjats:sup>−\u003C\u002Fjats:sup> CD27\u003Cjats:sup>−\u003C\u002Fjats:sup> T cells. In contrast, the reduced telomerase activity in these cells was not altered by blockade of PDL1\u002F2. We also demonstrate that PD‐1 signalling can inhibit the proliferative response in primary human CD8\u003Cjats:sup>+\u003C\u002Fjats:sup> T cells from both young and older humans. These data collectively highlight that some, but not all, functional changes that arise during progressive T‐cell differentiation and during ageing are maintained actively by inhibitory receptor signalling.\u003C\u002Fjats:p>",{"EN":1042},"Reversal of functional defects in highly differentiated young and old CD8 T cells by PDL blockade",{"VOID":1044},"22211948",{"VOID":1046},"10.1111\u002Fj.1365-2567.2011.03550.x","2025-02-02T23:23:11.234+00:00",[192],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1365-2567.2011.03550.x",[1051,1073,1090,1107],{"id":1052,"sortIndex":24,"researcher":23,"roles":1053,"affiliations":1054,"properties":1066},"f409c202-db46-4e69-9e3e-d6cbdefa0414",[],[1055],{"id":1056,"sortIndex":24,"affiliation":1057,"properties":23},"cea42fb9-8f8a-490d-be34-7c26b4b6f2cc",{"id":1058,"createTime":1059,"updateTime":1060,"relativeEntities":1061,"slug":1062,"properties":1063,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"e9006503-fee0-4fe7-88f0-e4a9ed1bc0a7","2024-01-10T21:19:43.241+00:00","2025-02-02T23:23:11.279+00:00",[],"Division-of-Infection-Immunity-University-College-London-London-UK",{"title":1064},{"VI":1065},"Division of Infection & Immunity, University College London, London, UK",{"openalex":1067,"orcid":1069,"title":1071},{"VOID":1068},"A5082859602",{"VOID":1070},"https:\u002F\u002Forcid.org\u002F0000-0003-1893-4912",{"EN":1072},"Siân M. 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expressing indoleamine 2,3‐dioxygenase (IDO), an enzyme which catabolizes tryptophan, prevent T‐cell proliferation \u003Cjats:italic>in vitro\u003C\u002Fjats:italic>, suppress maternal antifetal immunity during pregnancy and inhibit T‐cell‐mediated responses to tumour‐associated antigens. To examine the mechanistic basis of these phenomena we activated naïve murine T cells in chemically defined tryptophan‐free media. Under these conditions T cells expressed CD25 and CD69 and progressed through the first 12 hr of G0\u002FG1 phase but did not express CD71, cyclin D3, cdk4, begin DNA synthesis, or differentiate into cytotoxic effector cells. In addition, activated T cells with their growth arrested by tryptophan deprivation exhibited enhanced tendencies to die via apoptosis when exposed to anti‐Fas antibodies. Apoptosis was inhibited by caspase inhibitor and was not observed when T cells originated from Fas‐deficient mice. These findings suggest that T cells activated in the absence of free tryptophan entered the cell cycle but cell cycle progression ceased in mid‐G1 phase and T cells became susceptible to death via apoptosis, in part though Fas‐mediated signalling. 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Effect of collagen, Biochem J, 50, 421, 10.1042\u002Fbj2500421",{"doi":2856},"10.1042\u002Fbj2500421",{"id":23,"text":2858,"url":23,"identifiers":2859},"10.1084\u002Fjem.20021378",{"doi":2858},{"id":23,"text":2861,"url":23,"identifiers":2862},"10.1016\u002FS1074-7613(02)00480-6",{"doi":2861},{"id":23,"text":2864,"url":23,"identifiers":2865},"Pietras K, 2001, Inhibition of platelet‐derived growth factor receptors reduces interstitial hypertension and increases transcapillary transport in tumors, Cancer Res, 1, 2929",{},{"id":23,"text":2867,"url":23,"identifiers":2868},"10.1016\u002FS1074-7613(03)00113-4",{"doi":2867},{"id":23,"text":2870,"url":23,"identifiers":2871},"10.1084\u002Fjem.20050463",{"doi":2870},{"id":23,"text":2873,"url":23,"identifiers":2874},"10.1046\u002Fj.1440-1711.2002.01115.x",{"doi":2873},{"id":2876,"createTime":2877,"updateTime":2877,"relativeEntities":2878,"slug":2879,"properties":2880,"entityType":188,"verifyStatus":189,"verifyTime":2877,"verifyNote":190,"syncStatus":22,"languages":2896,"translateLanguages":23,"viewCount":24,"primaryUrl":2897,"fullTextUrl":23,"authors":2898,"publicationType":365,"publisherRelationship":2983,"citationCount":2481,"citationInfo":3020,"publishDate":3022,"publishYear":3023,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":3024,"isForceReanalyzing":535},"11a1ef05-159c-4ec2-8c7c-05e094dd0bc4","2024-09-20T22:22:01.978+00:00",[],"Studies-on-transcriptional-regulation-of-the-mucosal-T-cell-integrin-%CE%B1E%CE%B27-CD103-",{"mag":2881,"keywords":2883,"pmc":2884,"openalex":2886,"abstract":2888,"title":2890,"pm":2892,"doi":2894},{"VOID":2882},"1686260684",{},{"VOID":2885},"1783235",{"VOID":2887},"W1686260684",{"EN":2889},"\u003Cjats:title>Summary\u003C\u002Fjats:title>\u003Cjats:p>Integrin αEβ7 is expressed almost exclusively by mucosal T cells and mucosal dendritic antigen‐presenting cells (APCs) and is thought to be induced locally by transforming growth factor‐β (TGF‐β). In mice, mRNA for the αE subunit was found to be abundant in mucosal T cells but absent from other tissues. Exposure of a T‐cell line to TGF‐β strongly up‐regulated αE mRNA levels within 30 min, and nuclear run‐on experiments established that regulation occurred at the level of transcription. The organization of the human αE gene and a very closely linked novel gene, ELG, was determined. The αE promoter was tested in T cells and fibroblasts and functioned equally well in both cell types and did not confer TGF‐β responsiveness. Regions of the promoter providing enhancer activity and phorbol 12‐myristate 13‐acetate (PMA) responsiveness were identified by deletion studies. DNAse 1 hypersensitivity analysis of 36 kb of the αE gene revealed one hypersensitive site, found only in αE\u003Cjats:sup>+\u003C\u002Fjats:sup> cells, located near the transcription start points. These results show that, unlike the situation with other integrins, lineage specificity and cytokine responsiveness of αE transcription are not conferred by the proximal promoter. Specificity may depend on distant control elements that have not yet been identified.\u003C\u002Fjats:p>",{"EN":2891},"Studies on transcriptional regulation of the mucosal T‐cell integrin αEβ7 (CD103)",{"VOID":2893},"11412301",{"VOID":2895},"10.1046\u002Fj.1365-2567.2001.01232.x",[192],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1046\u002Fj.1365-2567.2001.01232.x",[2899,2919,2936,2953,2968],{"id":2900,"sortIndex":117,"researcher":23,"roles":2901,"affiliations":2902,"properties":2914},"e40ee1af-6fa3-45de-a74a-7ccb759fee7f",[],[2903],{"id":2904,"sortIndex":24,"affiliation":2905,"properties":23},"740b4249-9c5b-47da-80fa-f24db1731771",{"id":2906,"createTime":2907,"updateTime":2908,"relativeEntities":2909,"slug":2910,"properties":2911,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"5bac2c3c-bf3c-44e8-a269-bb42091ca54b","2024-02-10T15:07:56.556+00:00","2024-09-20T22:22:01.994+00:00",[],"The-Babraham-Institute-Babraham-Cambridge-UK",{"title":2912},{"VI":2913},"The Babraham Institute, Babraham, Cambridge, UK",{"openalex":2915,"title":2917},{"VOID":2916},"A5082117837",{"EN":2918},"Peter J. 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In oral mucosa and skin IEL express αeβ7 and the cutaneous lymphocyte‐associated antigen (CLA) but the mechanisms of adhesion of these subsets to keratinocytes are unknown. Levels of αeβ7 and CLA were up‐regulated on peripheral blood lymphocytes (PBL) by transforming growth factor‐β (TGF‐β) and interleukin‐12 (IL‐12), respectively, and both groups of lymphocytes adhered onto oral and skin keratinocytes. Adhesion of IL‐12‐activated PBL was totally abolished by anti‐lymphocyte‐associated function antigen type 1 (anti‐LFA‐1) antibodies but was unaffected by anti‐αeβ7 antibodies indicating that adhesion of the CLA‐positive subset is mediated via LFA‐1 interaction with intercellular adhesion molecule‐1 (ICAM‐1). Adhesion of TGF‐β‐activated PBL to E‐cadherin‐positive oral and skin keratinocytes was partially inhibited by anti‐αeβ7 antibodies but was unaffected by the blocking antibody E4.6 against E‐cadherin which detects the binding site for αeβ7‐positive lymphocytes in breast and gut epithelium. TGF‐β‐activated PBL also bound to an E‐cadherin‐negative oral keratinocyte cell line and adhesion was inhibited by anti‐αeβ7 antibodies. These results strongly suggest that in oral epithelium and epidermis αeβ7‐positive lymphocytes do not bind to E‐cadherin and there may be a novel second ligand for the αeβ7 integrin.\u003C\u002Fjats:p>",{"EN":3171},"Mechanisms of binding of cutaneous lymphocyte‐associated antigen‐positive and αeβ7‐positive lymphocytes to oral and skin keratinocytes",{"VOID":3173},"10469228",{"VOID":3175},"10.1046\u002Fj.1365-2567.1999.00855.x",[192],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1046\u002Fj.1365-2567.1999.00855.x",[3179,3198,3219,3236,3253,3274,3289],{"id":3180,"sortIndex":62,"researcher":23,"roles":3181,"affiliations":3182,"properties":3193},"c8302699-a5b0-4b0f-ac4e-9772a428da30",[],[3183],{"id":3184,"sortIndex":24,"affiliation":3185,"properties":23},"5cc10f8c-9efb-481f-93fd-a1b347dd4d8e",{"id":3186,"createTime":3187,"updateTime":3187,"relativeEntities":3188,"slug":3189,"properties":3190,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"99baf64f-ec4e-4957-af89-072ada001798","2024-09-20T22:21:50.343+00:00",[],"Department-of-Oral-Pathology-St-Bartholomew-s-the-Royal-London-School-of-Medicine-and-Dentistry-London",{"title":3191},{"EN":3192},"Department of Oral Pathology, St Bartholomew's & the Royal London School of Medicine and Dentistry, London",{"openalex":3194,"title":3196},{"VOID":3195},"A5096752957",{"EN":3197},"Farthing",{"id":3199,"sortIndex":117,"researcher":23,"roles":3200,"affiliations":3201,"properties":3212},"a577f037-f8b3-4c08-8e68-2ece1cb9129e",[],[3202],{"id":3203,"sortIndex":24,"affiliation":3204,"properties":23},"a06fa378-0b59-45cc-a6da-261ef63f5de3",{"id":3205,"createTime":3206,"updateTime":3206,"relativeEntities":3207,"slug":3208,"properties":3209,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"c5250d21-b1f4-4668-a786-308fbe05a0a1","2024-09-20T22:21:50.448+00:00",[],"Clinical-Academic-Group-of-Oral-Medicine-and-Dental-Diagnostic-Science-University-Dental-Hospital-Manchester-Manchester-UK",{"title":3210},{"EN":3211},"Clinical Academic Group of Oral Medicine and Dental Diagnostic Science, University Dental Hospital Manchester, Manchester, UK",{"openalex":3213,"orcid":3215,"title":3217},{"VOID":3214},"A5100703995",{"VOID":3216},"https:\u002F\u002Forcid.org\u002F0000-0002-2810-5758",{"EN":3218},"Chi Kong Li",{"id":3220,"sortIndex":24,"researcher":23,"roles":3221,"affiliations":3222,"properties":3229},"1d663c3f-25b8-4a93-acc0-1a94ea05049c",[],[3223],{"id":3224,"sortIndex":24,"affiliation":3225,"properties":23},"9c9e27ce-2245-49d7-a251-6de265ba9f9e",{"id":3186,"createTime":3187,"updateTime":3187,"relativeEntities":3226,"slug":3189,"properties":3227,"entityType":51,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":3228},{"EN":3192},{"openalex":3230,"orcid":3232,"title":3234},{"VOID":3231},"A5100370130",{"VOID":3233},"https:\u002F\u002Forcid.org\u002F0000-0002-9820-5738",{"EN":3235},"Todd M. 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