Macrophage migration inhibitory factor polymorphism (rs755622) in alopecia areata: a possible role in disease prevention

Rajabi, Fateme; Amoli, Mahsa M.; Robati, Reza M.; Almasi‐Nasrabadi, Mina; Jabalameli, Navid

doi:10.1007/s00403-019-01934-9

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…This might be achieved by gene therapy or direct injection of specific IP‐modulating products (Table 5). Research points towards a relationship between AA and genes coding for MHC II and to a lesser extent MHC I, NKG2D/ULBP3, 35,103 MIF, 345 AIRE, 191,192 FOXP3 197 and CTLA‐4 294‐296 . Gene therapies could be topically targeted to HFs to modulate expression, 346 and preliminary studies with nanoparticle delivery to AA‐affected follicles are promising 347 .…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

182

157

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Anagen stage hair follicles (HFs) exhibit “immune privilege (IP)” from the level of the bulge downwards to the bulb. Both passive and active IP mechanisms protect HFs from physiologically undesired immune responses and limit immune surveillance. IP is relative, not absolute, and is primarily based on absent, or greatly reduced, intra‐follicular antigen presentation via MHC class I and II molecules, along with prominent expression of “no danger” signals like CD200 and the creation of an immunoinhibitory signalling milieu generated by the secretory activities of HFs. Perifollicular mast cells, Tregs and other immunocytes may also contribute to HF IP maintenance in healthy human skin. Collapse of anagen hair bulb IP is an essential prerequisite for the development of alopecia areata (AA). In AA, lesional HFs are rapidly infiltrated by NKG2D + T cells and natural killer (NK) cells, while perifollicular mast cells acquire a profoundly pro‐inflammatory phenotype and interact with autoreactive CD8+ T cells. Using animal models, significant functional evidence has accumulated that demonstrates the dominance of the immune system in AA pathogenesis. Purified CD8+T‐cell and NK cell populations alone, which secrete fγ, suffice to induce the AA phenotype, while CD4+T‐cells aggravate it, and Tregs and iNKT cells may provide relative protection against AA development. While IP collapse may be induced by exogenous agents, inherent IP deficiencies might confer increased susceptibility to AA for some individuals. Thus, a key goal for effective AA management is the re‐establishment of a functional HF IP, which will also provide superior protection from disease relapse.

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Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

182

157

View full text Add to dashboard Cite

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“…Anahtar Kelimeler: Alopesi areata, CTLA4, Bağışıklık, PCR-RFLP , Analyses of CTLA4 Gene +49 A/G and CT 60 A/G Polymorphisms in Alopecia Areata Patients,Sabuncuoglu Serefeddin Health Science,5(2),[29][30][31][32][33][34][35][36][37][38] part of the body (Yazıcı et al, 2006;Alzolibnani, 2011;Rajabi et al, 2019;Rajabi et al 2022). The frequency of AA, which is alopecia totalis (AT) in which all hair is shed and alopecia universalis (AU) in which all body hair is involved, varies according to ethnic groups, is about 0.1% worldwide.…”

Section: öZetmentioning

confidence: 99%

Analysis of Ctla 4 Gene +49a/G and Ct60 a/G Polymorphisms in Alopecia Areata Patients

BOZKURT,

ŞAHİN,

SEZER SONDAŞ

et al. 2023

Sabuncuoglu Serefeddin Health Sciences

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Abstract Alopecia areata (AA) is a common, has organ-specific semptoms and an autoimmune disease that targets hair follicles and causes scarring, hair or hair loss. Although the etiopathogenesis of AA has not been clarified yet; In addition to attitude, psychological factors and persistence factors, autoimmune and inflammatory cells have a polygenic character in which genes are effective. Immunological hair follicle dysfunction process in AA are controlled by activated T cells. It is thought that cytokines released in T cells may cause hair loss in AA. Studies have reported that various genes of the immune system, such as interleukin and cytotoxic T lymphocyte-associated antigen 4 (CTLA4), are effective in the development of the cell membrane, and dysfunction of the CTLA-4 antigen may be associated with various diseases. The CTLA-4 gene polymorphism is thought to be associated with impaired control of T cell proliferation, and this gene is thought to be a candidate gene for susceptibility to autoimmunity. This study was conducted to investigate whether CTLA4 CT60 A/G and +49AG polymorphisms have a role in susceptibility to Alopecia Areata. 195 patients and 173 healthy volunteer controls were included in the study, and genotype and allele frequencies were determined by PCR-RFLP method. The obtained data were analyzed with OpenEpi. Our results showed that the +49AG polymorphism was not associated with AA susceptibility in the Turkish population, but the CT60 polymorphism might be associated with AA susceptibility. However, more studies are needed to confirm our results. Key Words: Alopecia areata, CTLA4, Immunity, PCR-RFLP Özet Alopesi areata (AA), saç foliküllerini hedef alan ve yara izi, saç veya saç dökülmesine neden olan yaygın, otoimmün bir hastalıktır. AA'nın etyopatogenezi henüz netlik kazanmamış olmakla birlikte; Tutum, psikolojik faktörler ve kalıcılık faktörlerine ek olarak, otoimmün ve enflamatuar hücreler, genlerin etkili olduğu poligenik bir karaktere sahiptir. AA'daki kıl folikülü disfonksiyon mekanizmaları immünolojiktir ve aktifleştirilmiş T hücreleri tarafından kontrol edilir. T hücrelerinde salınan sitokinlerin AA'da saç dökülmesine neden olabileceği düşünülmektedir. Çalışmalar, interlökin ve sitotoksik T lenfosit ilişkili antijen 4 (CTLA4) gibi bağışıklık sisteminin çeşitli genlerinin hücre zarının gelişiminde etkili olduğunu ve CTLA-4 antijeninin işlev bozukluğunun çeşitli hastalıklarla ilişkili olabileceğini bildirmiştir. . CTLA-4 gen polimorfizminin, T hücre proliferasyonunun bozulmuş kontrolü ile ilişkili olduğu ve bu genin otoimmüniteye yatkınlık için aday bir gen olduğu düşünülmektedir. Bu çalışma, CTLA4 +49AG ve CT60 polimorfizmlerinin Alopesi Areata'ya duyarlılıkta rolü olup olmadığını araştırmak amacıyla yapılmıştır. 195 hasta ve 173 sağlıklı kontrol çalışmaya dahil edildi ve genotip ve alel frekansları PCR-RFLP yöntemi ile belirlendi. Elde edilen veriler OpenEpi ile analiz edilmiştir. Sonuçlarımız, Türk popülasyonunda +49AG polimorfizminin AA duyarlılığı ile ilişkili olmadığını, ancak CT60 polimorfizminin AA duyarlılığı ile ilişkili olabileceğini göstermiştir. Ancak, sonuçlarımızı doğrulamak için daha fazla çalışmaya ihtiyaç vardır. Anahtar Kelimeler: Alopesi areata, CTLA4, Bağışıklık, PCR-RFLP

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