prikaz prve stranice dokumenta MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency
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Scientific paper - Original scientific paper
MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency
Blood, 107 (2006), 4; 1434-1444. urn:nbn:hr:184:886896
Buch, Thorsten; Polić, Bojan; Clausen, Bjoern E.; Weiss, Susanne; Akilli, Ozlem; Chang, Cheong-Hee; Flavell, Richard; Schulz, Ansgar; Jonjić, Stipan; Waisman, Ari; Foerster, Irmgard

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Buch, T., Polić, B., Clausen, B. E., Weiss, S., Akilli, O., Chang, C. H. ... Foerster, I. (2006). MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency. Blood, 107. (4), 1434-1444. Retrieved from https://urn.nsk.hr/urn:nbn:hr:184:886896

Buch, Thorsten, et al. "MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency." Blood, vol. 107, no. 4, 2006, pp. 1434-1444. https://urn.nsk.hr/urn:nbn:hr:184:886896

Buch, Thorsten, Bojan Polić, Bjoern E. Clausen, Susanne Weiss, Ozlem Akilli, Cheong Hee Chang, Richard Flavell, et al. "MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency." Blood 107, no. 4 (2006): 1434-1444. https://urn.nsk.hr/urn:nbn:hr:184:886896

Buch, T., et al. (2006) 'MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency', Blood, 107(4), pp. 1434-1444. Available at: https://urn.nsk.hr/urn:nbn:hr:184:886896 (Accessed 25 December 2024)

Buch T, Polić B, Clausen BE, Weiss S, Akilli O, Chang CH, and sur.. MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency. Blood [Internet]. 2006 [cited 2024 December 25];107(4):1434-1444. Available at: https://urn.nsk.hr/urn:nbn:hr:184:886896

T. Buch, et al., "MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency", Blood, vol. 107, no. 4, pp. 1434-1444, 2006. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:886896. [Accessed: 25 December 2024]

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Metadata
Title (english)MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses: implications for MHC class II deficiency
Title (english)MHC class II expression through a hitherto unknown pathway supports T helper cell dependent immune responses:implications for MHC class II deficiency
AuthorThorsten Buch
AuthorBojan Polić
AuthorBjoern E. Clausen
AuthorSusanne Weiss
AuthorOzlem Akilli
AuthorCheong-Hee Chang
AuthorRichard Flavell
AuthorAnsgar Schulz
AuthorStipan Jonjić
AuthorAri Waisman
AuthorIrmgard Foerster
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Clinical Medical Sciences
Scientific / art field,
discipline and subdiscipline		NATURAL SCIENCES
Biology
Abstract (english)
MHC class II (MHCII) deficiency of Bare Lymphocyte Syndrome (BLS) is a severe immunodeficiency characterized by deficient T helper (Th) cell dependent immunity. The disease is caused by defects of the MHCII promoter complex resulting in low or absent MHCII expression. We demonstrate in a murine model of MHCII deficiency (RFX5- or CIITA-deficient mice) that residual MHCII expression by professional APC is sufficient to support activation of adoptively transferred Th cells. Furthermore, upon transplantation of WT thymic epithelium we observed development of endogenous Th cells with restoration of Th cell dependent antibody responses and immunity to cytomegalovirus infection, thus opening the posssibility of an alternative treatment regimen for BLS. Residual MHCII expression was further induced by the presence of Th cells and also other stimuli. Analysis of CIITA/RFX5 double deficient animals revealed that this inducible MHCII expression is genetically independent of the known promoter complex and thus constitutes an alternative MHCII expression pathway. In these experiments, we also detected a novel repressive function of the RFX complex in the absence of CIITA.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleBlood
Numberingvol. 107, no. 4, pp. 1434-1444
p-ISSN0006-4971
URN:NBNurn:nbn:hr:184:886896
Publication2006
Document URLhttp://bib.irb.hr/212837
Type of resourceText
Access conditionsClosed access
Terms of useLicence In copyright icon
Created on2020-02-04 17:08:50