Apoptosis resistance in peripheral blood lymphocytes of alopecia areata patients

Zöller, Margot; McElwee, Kevin J.; Vitacolonna, Mario; Hoffmann, Rolf

doi:10.1016/j.jaut.2004.08.002

Cited by 33 publications

(27 citation statements)

References 70 publications

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“…As there is also increasing evidence that AA is a tissue-specific autoimmune disease [4], it is reasonable to assume that immunologic factors trigger the disease in genetically susceptible populations. A Th1-dominant cytokine imbalance is observed in sera of severe AA patients and peripheral blood lymphocytes of progressive AA patients are resistant to apoptosis [23, 24]. The collapse of immune privilege of anagen hair follicles, which is sustained by very low levels of MHC class I expression, may also be crucial for the pathogenesis of AA [4, 25, 26].…”

Section: Discussionmentioning

confidence: 99%

Pulse Corticosteroid Therapy for Alopecia Areata: Study of 139 Patients

Nakajima

Inui

Itami³

2007

Dermatology

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Background/Aim: Recent reports of pulse corticosteroid therapy for alopecia areata (AA) show its efficacy for patients with a history of ≤1 year but not for recalcitrant cases or alopecia totalis/universalis. The purpose of this study was to evaluate the efficacy and safety of pulse corticosteroid therapy for recent-onset AA patients. Method: A total of 139 severe AA patients aged >15 years were included in this study. The duration from the onset of active hair loss was within 12 months for 125 (89.9%) of those patients. Results: Of the patients, 72.7% had hair loss on >50% of their scalp area. Among the recent-onset group (duration of AA ≤6 months), 59.4% were good responders (>75% regrowth of alopecia lesions), while 15.8% with >6 months duration showed a good response. Recent-onset AA patients with less severe disease (≤50% hair loss) responded at a rate of 88.0%, but only 21.4% of recent-onset patients with 100% hair loss responded. No serious adverse effects were observed.

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Section: Discussionmentioning

confidence: 99%

Pulse Corticosteroid Therapy for Alopecia Areata: Study of 139 Patients

Nakajima

Inui

Itami³

2007

Dermatology

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“…Apoptosis was evaluated by PI staining in hypotonic solution and analyzed by flow cytometry as described by Nicoletti et al 37 Shown are FACS data from one out of three experiments CD44v7 ligation induces apoptosis U Hoffmann et al autoimmune disease, inflammatory infiltrates are composed mainly of CD25/CD154-positive CD4 T cells that express CD44v7 and display increased resistance towards apoptosis. 29 In the mouse model of alopecia areata, 30 apoptosis resistance was accompanied by Bcl-2 and Bcl-XL upregulation. Although not analyzed, it is tempting to speculate that anti-CD44v7 antibody might induce apoptosis in these infiltrates too.…”

Section: Discussionmentioning

confidence: 99%

CD44v7 ligation downregulates the inflammatory immune response in Crohn's disease patients by apoptosis induction in mononuclear cells from the lamina propria

et al. 2007

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Deletion of exon CD44v7 abrogates experimental colitis by apoptosis induction in intestinal mononuclear cells. Here we show that CD44v7 expression was upregulated upon CD40 ligation in human mononuclear cells, and examined whether ligation of CD44v7 also affects activation and apoptosis in lamina propria mononuclear cells (LPMC) from Crohn's disease (CD) patients. Thirty five patients with chronic inflammatory bowel disease (IBD), fourteen controls and four patients with diverticulitis were evaluated. CD44v7 was upregulated predominantly in the inflamed mucosa of CD patients. Furthermore, incubation with an antiCD44v7 antibody induced apoptosis in LPMC isolated from inflamed mucosa of CD patients, but not from non-inflamed mucosa, from patients with ulcerative colitis (UC) or from normal controls. CD40 ligation and simultaneous incubation with anti-CD44v7 significantly downregulated CD80 in dendritic cells, thus inhibiting a critical second signal for naive T-cell activation. The apoptotic signal was mediated via the intrinsic mitochondrial pathway with decreased Bcl-2 and increased 7A6 (a mitochondrial membrane protein) expression. It was Fas independent and required caspases-3 and -9 activation. The process is highly specific for macrophage activation via CD40. These findings point to a novel mechanism of apoptosis induction in CD patients mediated by CD44v7 ligation.

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“…In this regard, TL resistance against apoptosis may contribute to inappropriate autoreactive TL accumulation, thereby participating in hair loss [12,13]; invasion of TLs may trigger apoptosis, perhaps via Fas/Fas ligand and granzyme B pathways, possibly playing an important role in the induction and persistence of chronic alopecia areata [11,14,15]. Specifically, the most prominent cells located in or around the hair follicle include CD4 + and CD8 + TLs, and hair loss requires a collaboration between CD8 + and CD4 + TLs [16,17].…”

Section: Discussionmentioning

confidence: 99%