RGD Reference Report - Proinflammatory Th17 cells are expanded and induced by dendritic cells in spondylarthritis-prone HLA-B27-transgenic rats. - Rat Genome Database

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Proinflammatory Th17 cells are expanded and induced by dendritic cells in spondylarthritis-prone HLA-B27-transgenic rats.

Authors: Glatigny, S  Fert, I  Blaton, MA  Lories, RJ  Araujo, LM  Chiocchia, G  Breban, M 
Citation: Glatigny S, etal., Arthritis Rheum. 2012 Jan;64(1):110-20. doi: 10.1002/art.33321.
RGD ID: 9068946
Pubmed: PMID:21905004   (View Abstract at PubMed)
DOI: DOI:10.1002/art.33321   (Journal Full-text)

OBJECTIVE: HLA-B27/human beta2-microglobulin-transgenic (B27-transgenic) rats, a model of spondylarthritis (SpA), develop spontaneous colitis and arthritis under conventional conditions. CD4+ T cells are pivotal in the development of inflammation in B27-transgenic rats. This study was undertaken to characterize the phenotype of CD4+ T cells in this model and to determine whether dendritic cells (DCs) induce proinflammatory T cells. METHODS: The phenotype of CD4+ T cells from rat lymph nodes (LNs) draining the sites of inflammation was analyzed by flow cytometry. Immunostaining was used to detect interleukin-17 (IL-17)-producing cells in the rat joints. DCs from B27-transgenic or control rats (transgenic for HLA-B7 or nontransgenic) were cocultured with control CD4+ T cells and stimulated with anti-T cell receptor alpha/beta. RESULTS: IL-17A- and tumor necrosis factor alpha (TNFalpha)-producing CD4+ T cells were expanded in mesenteric and popliteal LNs from B27-transgenic rats. The accumulation of Th17 cells correlated with disease development, in contrast to Th1 or Treg cells. IL-17-positive mononuclear cells were detected in the arthritic joints of B27-transgenic rats but not in the joints of control rats. Finally, in vitro cocultures demonstrated that Th17 cells were preferentially induced and expanded by DCs from B27-transgenic rats, by a process that may involve defective engagement of costimulatory molecules. CONCLUSION: Our findings indicate that expanded CD4+ T cells in B27-transgenic rats exhibit a proinflammatory Th17 phenotype characterized by IL-17A and TNFalpha production. Furthermore, this population is preferentially induced by DCs from B27-transgenic rats. These data point toward an induction of Th17 cells as a possible pathogenic mechanism in this model of SpA. However, their pathogenic role still needs to be shown.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
IL17AHumanSpondylarthritis  ISOIl17a (Rattus norvegicus)protein:increased expression:serum (rat)RGD 
Il17aRatSpondylarthritis  IEP protein:increased expression:serum (rat)RGD 
Il17aMouseSpondylarthritis  ISOIl17a (Rattus norvegicus)protein:increased expression:serum (rat)RGD 


Genes (Rattus norvegicus)
Il17a  (interleukin 17A)

Genes (Mus musculus)
Il17a  (interleukin 17A)

Genes (Homo sapiens)
IL17A  (interleukin 17A)