Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis

Sumii, Koji; Sun, Xun; Oyamada, Akiko; Yamada, Hisakata; Kira, Jun Ichi; Yoshikai, Yasunobu

doi:10.1016/j.jneuroim.2015.12.005

Cited by 6 publications

(4 citation statements)

References 30 publications

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“…Similarly, previous studies demonstrated that CD30 + T cells are involved in the pathogenesis of several granulomatous inflammatory diseases [ 26 – 28 ]. Recently, Shinoda et al [ 29 ] demonstrated that CD30 knockout mice showed milder symptoms in a model of experimental autoimmune encephalomyelitis and less antigen-specific Th1 and Th17 cells were induced. These findings suggest that CD30 expression on CD4 + T cells is implicated in the pathogenesis of autoimmune diseases of the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

Soluble cytokine receptor levels in aqueous humour of patients with specific autoimmune uveitic entities: sCD30 is a biomarker of granulomatous uveitis

El‐Asrar

Berghmans

Al-Obeidan

et al. 2019

Eye

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Purpose Soluble cytokine receptors are potential biomarkers for immune activation and have a promising potential as immunotherapeutic agents. We investigated the levels of soluble cytokine receptors in aqueous humour (AH) samples from patients with specific autoimmune uveitic entities. Methods Patients with active uveitis associated with Behçet’s disease (BD) ( n = 13), sarcoidosis ( n = 8), HLA-B27-related inflammation ( n = 12), Vogt–Koyanagi–Harada (VKH) disease ( n = 12) and control subjects ( n = 9) were included. AH samples were analyzed with the use of multiplex assays for the proinflammatory cytokine tumour necrosis factor (TNF)-α and the soluble cytokine receptors sCD30, sCD163, sgp130, sIL-6 receptor-α (sIL-6R), sTNFRI and sTNFRII. Results TNF-α and soluble cytokine receptor AH levels were significantly higher in uveitis patients ( n = 45) compared with controls ( n = 9). When nongranulomatous uveitis (BD and HLA-B27-associated uveitis) was compared with granulomatous uveitis (sarcoidosis and VKH disease), the levels of sCD30 and sTNFRI/TNF-α and sTNFRII/TNF-α ratios were significantly enhanced in granulomatous uveitis. Finally, when comparing the profile in the specific uveitis entities, sCD30 levels were highest in patients with VKH disease. sgp130, sCD163, sIL-6R, sTNFRI and sTNFRII did not differ significantly between the four different clinical uveitic subgroups. Conclusions Soluble cytokine receptors are significantly upregulated in autoimmune uveitis. CD30 + T cells might contribute to the inflammatory process in granulomatous uveitis, particularly in VKH disease. Granulomatous uveitis is also characterized by significantly higher sTNFRs/TNF-α ratios than nongranulomatous uveitis.

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Section: Discussionmentioning

confidence: 99%

Soluble cytokine receptor levels in aqueous humour of patients with specific autoimmune uveitic entities: sCD30 is a biomarker of granulomatous uveitis

El‐Asrar

Berghmans

Al-Obeidan

et al. 2019

Eye

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“…In vitro, CD30-deficient T cells displayed impaired Th17 differentiation and produced IL-2 under Th17 cell polarization conditions, indicating that CD30 ligation is needed to suppress IL-2 signaling during Th17 cell differentiation (290). Accordingly, CD30-deficient mice subjected to EAE induction exhibited reduced disease symptoms (367). With respect to Tregs, studies using a mouse model of acute GvHD showed that early CD30 signaling is important for the suppressive functionality of Tregs (484).…”

Section: Cd30/cd30lmentioning

confidence: 99%

The TNF Family of Ligands and Receptors: Communication Modules in the Immune System and Beyond

Dostert

Grusdat

Letellier

et al. 2019

Physiological Reviews

290

273

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The tumor necrosis factor (TNF) and TNF receptor (TNFR) superfamilies (TNFSF/TNFRSF) include 19 ligands and 29 receptors that play important roles in the modulation of cellular functions. The communication pathways mediated by TNFSF/TNFRSF are essential for numerous developmental, homeostatic, and stimulus-responsive processes in vivo. TNFSF/TNFRSF members regulate cellular differentiation, survival, and programmed death, but their most critical functions pertain to the immune system. Both innate and adaptive immune cells are controlled by TNFSF/TNFRSF members in a manner that is crucial for the coordination of various mechanisms driving either co-stimulation or co-inhibition of the immune response. Dysregulation of these same signaling pathways has been implicated in inflammatory and autoimmune diseases, highlighting the importance of their tight regulation. Investigation of the control of TNFSF/TNFRSF activities has led to the development of therapeutics with the potential to reduce chronic inflammation or promote anti-tumor immunity. The study of TNFSF/TNFRSF proteins has exploded over the last 30 yr, but there remains a need to better understand the fundamental mechanisms underlying the molecular pathways they mediate to design more effective anti-inflammatory and anti-cancer therapies.

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“…We selected 8-week-old and 10-to 13-month-old male mice as the young and aged models, respectively. Spp1-EGFP-KI mice, CD153 -/mice, Rag2 -/mice and CD30 -/mice were described previously (16,47,(54)(55)(56). For other experiments, we purchased 8-week-and 12-month-old male C57BL/6J mice from Japan SLC as respective young and aged mice.…”

Section: Animalsmentioning

confidence: 99%

CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

Sato¹,

Oguchi²,

Fukushima³

et al. 2022

Journal of Clinical Investigation

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Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153 + PD-1 + CD4 + senescence-associated T (SAT) cells and CD30 + T-bet + age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.

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Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis

Cited by 6 publications

References 30 publications

Soluble cytokine receptor levels in aqueous humour of patients with specific autoimmune uveitic entities: sCD30 is a biomarker of granulomatous uveitis

Soluble cytokine receptor levels in aqueous humour of patients with specific autoimmune uveitic entities: sCD30 is a biomarker of granulomatous uveitis

The TNF Family of Ligands and Receptors: Communication Modules in the Immune System and Beyond

CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

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