期刊
CURRENT OPINION IN RHEUMATOLOGY
卷 23, 期 1, 页码 43-49出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0b013e32833ee946
关键词
antigen-presenting cell; IFN-gamma; IL-17; T cell
类别
资金
- NIH [RO1 AR42527, RO1 AI44142, RO1 EY11916, RO1 AI 57266, PO1 HL 058000]
- Vasculitis Foundation
- NATIONAL EYE INSTITUTE [R01EY011916] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL129941, P01HL058000] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI057266, R01AI044142] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR042527] Funding Source: NIH RePORTER
Purpose of review Granuloma formation in giant cell arteritis (GCA) emphasizes the role of adaptive immunity and highlights the role of antigen-specific T cells. Recent data demonstrate that at least two separate lineages of CD4 T cells participate in vascular inflammation, providing an important clue that multiple disease instigators may initiate pathogenic immunity. Recent finding IFN-gamma-producing Th1 cells and IL-17-producing Th17 cells have been implicated in GCA. Patients with biopsy-positive GCA underwent two consecutive temporal artery biopsies, one prior to therapy and one while on corticosteroids. In untreated patients, Th1 and Th17 cells co-existed in the vascular lesions. Following therapy, Th17 cells were essentially lost, whereas Th1 cells persisted almost unaffected. In the peripheral blood of untreated patients Th17 frequencies were increased eight-fold, but normalized with therapy. Blood Th1 cells were doubled in frequency, independent of therapy. Corticosteroids functioned by selectively suppressing IL-1 beta, IL-6 and IL-23-releasing antigen-presenting cells (APCs), disrupting induction of Th17 cells. Summary At least two distinct CD4 T-cell subsets promote vascular inflammation in GCA. In early disease, APCs promote differentiation of Th17 as well as Th1 cells. Chronic disease is characterized by persistent Th1-inducing signals, independent of IL-17-mediated inflammation. More than one disease instigator may trigger APCs to induce multiple T-cell lineages. Cocktails of therapies will be needed for appropriate disease control.
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