Alopecia Areata After Vaccination: Recurrence with Rechallenge

Chu, Chia-Hui; Cheng, Yu-Pin; Chan, Jung-Yi

doi:10.1111/pde.12849

Cited by 33 publications

(30 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Others include vaccinations, febrile illness, and drugs. A low frequency of alopecia areata was reported to arise shortly after vaccinations against a variety of human pathogens including Japanese encephalitis 96 , hepatitis B virus 97 , Clostridium tetani 98 , herpes zoster virus 99 , and papillomavirus 100 . By contrast, one report showed that alopecia areata was triggered or exacerbated by swine flu virus infection 101 .…”

Section: Mechanisms/pathophysiologymentioning

confidence: 99%

Alopecia areata

Pratt

King

Messenger

et al. 2017

Nat Rev Dis Primers

580

528

View full text Add to dashboard Cite

Alopecia areata is an autoimmune disorder characterized by transient, non-scarring hair loss and preservation of the hair follicle. Hair loss can take many forms ranging from loss in well-defined patches to diffuse or total hair loss, which can affect all hair bearing sites. Patchy alopecia affecting the scalp is the most common type. Alopecia areata affects nearly 2% of the general population at some point during their lifetime. Skin biopsies of alopecia areata affected skin show a lymphocytic infiltrate in and around the bulb or the lower part of the hair follicle in anagen (hair growth) phase. A breakdown of immune privilege of the hair follicle is thought to be an important driver of alopecia areata. Genetic studies in patients and mouse models showed that alopecia areata is a complex, polygenic disease. Several genetic susceptibility loci were identified associated with signaling pathways that are important to hair follicle cycling and development. Alopecia areata is usually diagnosed based on clinical manifestations, but dermoscopy and histopathology can be helpful. Alopecia areata is difficult to manage medically, but recent advances in understanding the molecular mechanisms have revealed new treatments and the possibility of remission in the near future.

show abstract

Section: Mechanisms/pathophysiologymentioning

confidence: 99%

Alopecia areata

Pratt

King

Messenger

et al. 2017

Nat Rev Dis Primers

580

528

View full text Add to dashboard Cite

show abstract

“…Low incidence of alopecia areata has also been observed shortly after vaccinations against a variety of human pathogens including, hepatitis B virus [108], Clostridium tetani [109], herpes zoster virus [110], Japanese encephalitis [111] and human papillomavirus [112]. The disease in these cases may be a result of a hypersensitive reaction to vaccines in patients that are genetically predisposed.…”

Section: Infectious Agents Are Linked To Onset and Progression Of Alomentioning

confidence: 99%

Alopecia areata: A multifactorial autoimmune condition

Simakou

Butcher

Reid

et al. 2019

Journal of Autoimmunity

202

151

View full text Add to dashboard Cite

Highlights  Alopecia areata is a polygenic and multifactorial autoimmune disease characterised by non-scarring hair loss.  Autoreactive CD8 + , CD4 + , natural killer cells and plasmacytoid dendritic cells infiltrate around the hair follicles during the growth (anagen) phase.  Increased cytokine activity, particularly IFN-γ, results in disruption of the hair follicle immune privilege and premature termination of the anagen phase, followed by hair follicle atrophy and dystrophy in persistent disease.

show abstract

“…AA is one of the most common autoimmune diseases, with a lifetime incidence of 2·1% and prevalence of 0·1–0·2% . AA develops in genetically predisposed individuals, usually with no identifiable trigger factor, although viral infection, vaccination and psychological stress have been reported in association with disease onset . Hair loss caused by AA is sometimes considered solely a cosmetic problem, despite being associated with significant psychological distress and increased risk of developing inflammatory comorbidities .…”

mentioning

confidence: 99%

“…1,2 AA develops in genetically predisposed individuals, usually with no identifiable trigger factor, although viral infection, vaccination and psychological stress have been reported in association with disease onset. [3][4][5] Hair loss caused by AA is sometimes considered solely a cosmetic problem, despite being associated with significant psychological distress 6 and increased risk of developing inflammatory comorbidities. 7 Treatment options for AA include contact sensitizers or topical, intralesional or systemic steroids, but their efficacy is limited and treatment is commonly ineffective for extensive AA.…”

mentioning

confidence: 99%

Alopecia areata is characterized by dysregulation in systemic type 17 and type 2 cytokines, which may contribute to disease‐associated psychological morbidity

et al. 2019

View full text Add to dashboard Cite

Summary Background Alopecia areata (AA) is a common autoimmune disease, causing patchy hair loss that can progress to involve the entire scalp (totalis) or body (universalis). CD8+NKG2D+ T cells dominate hair follicle pathogenesis, but the specific mechanisms driving hair loss are not fully understood. Objectives To provide a detailed insight into the systemic cytokine signature associated with AA, and to assess the association between cytokines and depression. Methods We conducted multiplex analysis of plasma cytokines from patients with AA, patients with psoriatic arthritis (PsA) and healthy controls. We used the Hospital Anxiety and Depression Scale (HADS) to assess the occurrence of depression and anxiety in our cohort. Results Our analysis identified a systemic inflammatory signature associated with AA, characterized by elevated levels of interleukin (IL)‐17A, IL‐17F, IL‐21 and IL‐23 indicative of a type 17 immune response. Circulating levels of the type 2 cytokines IL‐33, IL‐31 and IL‐17E (IL‐25) were also significantly increased in AA. In comparison with PsA, AA was associated with higher levels of IL‐17F, IL‐17E and IL‐23. We hypothesized that circulating inflammatory cytokines may contribute to wider comorbidities associated with AA. Our assessment of psychiatric comorbidity in AA using HADS scores showed that 18% and 51% of people with AA experienced symptoms of depression and anxiety, respectively. Using linear regression modelling, we identified that levels of IL‐22 and IL‐17E are positively and significantly associated with depression. Conclusions Our data highlight changes in both type 17 and type 2 cytokines among people with AA, suggesting that complex systemic cytokine profiles may contribute both to the pathogenesis of AA and to the associated depression. What's already known about this topic? NKG2D+CD8+ T cells cause hair loss in alopecia areata (AA) but the immunological mechanisms underlying the disease are not fully understood. AA is associated with changes in levels of interleukin (IL)‐6, tumour necrosis factor‐α, IL‐1β and type 17 cytokines. Psychiatric comorbidity is common among people with AA. What does this study add? People with AA have increased plasma levels of the type 2 cytokines IL‐33, IL‐31 and IL‐17E (IL‐25), in addition to the type 17 cytokines IL‐17A, IL‐21, IL‐23 and IL‐17F. Levels of IL‐17E and IL‐22 positively predict depression score. What is the translational message? AA is associated with increased levels of multiple inflammatory cytokines, implicating both type 17‐ and type 2 immune pathways. Our data indicate that therapeutic strategies for treating AA may need to address the underlying type 17‐ and type 2 immune dysregulation, rather than focusing narrowly on the CD8+ T‐cell response. An immunological mechanism might contribute directly to the depression observed in people with AA.

show abstract

Alopecia Areata After Vaccination: Recurrence with Rechallenge

Cited by 33 publications

References 6 publications

Alopecia areata

Alopecia areata

Alopecia areata: A multifactorial autoimmune condition

Alopecia areata is characterized by dysregulation in systemic type 17 and type 2 cytokines, which may contribute to disease‐associated psychological morbidity

Contact Info

Product

Resources

About