Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis
Objective To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS). Methods Cohorts of male and female patients with AS and age‐ and sex‐matched healthy control subjects were selected, and the levels of serum cytokines (interferon‐γ [IFNγ], tumor necrosis factor α, inter...
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| Published in | Arthritis & rheumatology (Hoboken, N.J.) Vol. 68; no. 3; pp. 679 - 689 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wiley Subscription Services, Inc
01.03.2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 2326-5191 2326-5205 2326-5205 |
| DOI | 10.1002/art.39464 |
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| Abstract | Objective
To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).
Methods
Cohorts of male and female patients with AS and age‐ and sex‐matched healthy control subjects were selected, and the levels of serum cytokines (interferon‐γ [IFNγ], tumor necrosis factor α, interleukin‐17A [IL‐17A], and IL‐6) were examined by enzyme‐linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches.
Results
The frequency of IL‐17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS‐associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex‐related immune profiles were independent of HLA–B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS.
Conclusion
The results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex‐related differences in the clinical features of AS and could provide a rationale for sex‐specific treatment of AS. |
|---|---|
| AbstractList | Objective
To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).
Methods
Cohorts of male and female patients with AS and age‐ and sex‐matched healthy control subjects were selected, and the levels of serum cytokines (interferon‐γ [IFNγ], tumor necrosis factor α, interleukin‐17A [IL‐17A], and IL‐6) were examined by enzyme‐linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches.
Results
The frequency of IL‐17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS‐associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex‐related immune profiles were independent of HLA–B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS.
Conclusion
The results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex‐related differences in the clinical features of AS and could provide a rationale for sex‐specific treatment of AS. To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS). Cohorts of male and female patients with AS and age- and sex-matched healthy control subjects were selected, and the levels of serum cytokines (interferon-γ [IFNγ], tumor necrosis factor α, interleukin-17A [IL-17A], and IL-6) were examined by enzyme-linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches. The frequency of IL-17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS-associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex-related immune profiles were independent of HLA-B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS. The results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex-related differences in the clinical features of AS and could provide a rationale for sex-specific treatment of AS. To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).OBJECTIVETo identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).Cohorts of male and female patients with AS and age- and sex-matched healthy control subjects were selected, and the levels of serum cytokines (interferon-γ [IFNγ], tumor necrosis factor α, interleukin-17A [IL-17A], and IL-6) were examined by enzyme-linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches.METHODSCohorts of male and female patients with AS and age- and sex-matched healthy control subjects were selected, and the levels of serum cytokines (interferon-γ [IFNγ], tumor necrosis factor α, interleukin-17A [IL-17A], and IL-6) were examined by enzyme-linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches.The frequency of IL-17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS-associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex-related immune profiles were independent of HLA-B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS.RESULTSThe frequency of IL-17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS-associated alterations in the Th1 axis, such as the frequency of IFNγ and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex-related immune profiles were independent of HLA-B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS.The results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex-related differences in the clinical features of AS and could provide a rationale for sex-specific treatment of AS.CONCLUSIONThe results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex-related differences in the clinical features of AS and could provide a rationale for sex-specific treatment of AS. Objective To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS). Methods Cohorts of male and female patients with AS and age- and sex-matched healthy control subjects were selected, and the levels of serum cytokines (interferon-[gamma] [IFN[gamma]], tumor necrosis factor [alpha], interleukin-17A [IL-17A], and IL-6) were examined by enzyme-linked immunosorbent assay, the frequencies of Th1 and Th17 cells were assessed by flow cytometry, and whole blood gene expression was analyzed using both microarray and NanoString approaches. Results The frequency of IL-17A and Th17 cells, both of which are key factors in the inflammatory Th17 axis, was elevated in male patients with AS but not in female patients with AS. In contrast, AS-associated alterations in the Th1 axis, such as the frequency of IFN[gamma] and Th1 cells in serum, were independent of a patient's sex. Results of microarray analysis supported an altered Th17 axis in male patients, with a specific increase in IL17RA. In addition, male and female patients with AS displayed shared gene expression patterns, while male patients with AS had additional alterations in gene expression that were not seen in female patients with AS. The differential sex-related immune profiles were independent of HLA-B27 status, clinical disease activity (as measured by the Bath Ankylosing Spondylitis Disease Activity Index), or treatment (with nonsteroidal antiinflammatory drugs or biologic agents), implicating intrinsic sexual dimorphism in AS. Conclusion The results of this study demonstrate distinct sexual dimorphism in the activation status of the immune system in patients with AS, particularly in the Th17 axis. This dimorphism could underlie sex-related differences in the clinical features of AS and could provide a rationale for sex-specific treatment of AS. |
| Author | Green, Blerta Qaiyum, Zoya Yip, Paul Inman, Robert D. Gracey, Eric Yao, YuChen Baglaenko, Yuriy Lin, Aifeng Anton, Ammepa Ayearst, Renise |
| Author_xml | – sequence: 1 givenname: Eric surname: Gracey fullname: Gracey, Eric organization: University of Toronto, Toronto Western Hospital, and University Health Network – sequence: 2 givenname: YuChen surname: Yao fullname: Yao, YuChen organization: University of Toronto, Toronto Western Hospital, and University Health Network – sequence: 3 givenname: Blerta surname: Green fullname: Green, Blerta organization: Toronto Western Hospital and University Health Network – sequence: 4 givenname: Zoya surname: Qaiyum fullname: Qaiyum, Zoya organization: University of Toronto, Toronto Western Hospital, and University Health Network – sequence: 5 givenname: Yuriy surname: Baglaenko fullname: Baglaenko, Yuriy organization: University of Toronto, Toronto Western Hospital, and University Health Network – sequence: 6 givenname: Aifeng surname: Lin fullname: Lin, Aifeng organization: Toronto Western Hospital and University Health Network – sequence: 7 givenname: Ammepa surname: Anton fullname: Anton, Ammepa organization: Toronto Western Hospital and University Health Network – sequence: 8 givenname: Renise surname: Ayearst fullname: Ayearst, Renise organization: Toronto Western Hospital and University Health Network – sequence: 9 givenname: Paul surname: Yip fullname: Yip, Paul organization: University Health Network – sequence: 10 givenname: Robert D. surname: Inman fullname: Inman, Robert D. organization: University of Toronto, Toronto Western Hospital, and University Health Network |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26473967$$D View this record in MEDLINE/PubMed |
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| Snippet | Objective
To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).
Methods
Cohorts of male and female patients with AS and age‐... To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS). Cohorts of male and female patients with AS and age- and sex-matched... Objective To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS). Methods Cohorts of male and female patients with AS and age-... To identify an immunologic basis for the male sex bias in ankylosing spondylitis (AS).OBJECTIVETo identify an immunologic basis for the male sex bias in... |
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| SubjectTerms | Adult Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Gene Expression Humans Interferon-gamma - blood Interleukin-17 - blood Male Microarray Analysis Peptide Fragments - blood Polymerase Chain Reaction Reverse Transcription Sex Factors Spondylitis, Ankylosing - blood Spondylitis, Ankylosing - immunology Th1 Cells - pathology Th17 Cells - pathology Tumor Necrosis Factor-alpha - blood |
| Title | Sexual Dimorphism in the Th17 Signature of Ankylosing Spondylitis |
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