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| LETTER TO EDITOR |
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| Year : 2011 | Volume
: 3
| Issue : 1 | Page : 41-42 |
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Alopecia areata - probing the deforestation
Dilip Gude
Department of Internal Medicine, AMC, 3rd Floor, Medwin Hospital, Chirag Ali lane, Nampally, Hyderabad, Andhra Pradesh, India
| Date of Web Publication | 16-Jun-2011 |
Correspondence Address:
Dilip Gude
Registrar, Internal Medicine, AMC, 3rd Floor, Medwin Hospital, Chirag Ali lane, Nampally, Hyderabad, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0974-7753.82132
How to cite this article:
Gude D. Alopecia areata - probing the deforestation. Int J Trichol 2011;3:41-2 |
Sir,
Alopecia areata (AA) is a chronic inflammatory auto-immune disorder resulting in nonscarring hair loss. It is thought to be triggered by a collapse of immune privilege in hair follicles. The dominant role of Th1 cells is explained by the demonstration of infiltrating chemokine (C-C motif) receptor 5 (CCR5+) CD4 + T lymphocytes around hair follicles. Intralesional injections of both IL-4 and neutralizing anti-IFN-γ antibody have shown to suppress CD8+ T cell infiltrates around the hair follicles and repressed enhanced IFN-γ mRNA expression in the affected alopecic skin. Also Th1 transcription factor T-box21 (T-bet) small interfering RNAs (siRNA) mitigated alopecia and resulted in the restoration of hair shaft elongation. [1]
Peripheral blood gene expression profiling of AA showed upregulation in immune response, cytokine signaling, signal transduction, cell cycle, proteolysis and cell adhesion-related genes. It also revealed the activation of several genes related to natural killer-cell cytotoxicity, apoptosis, mitogen activated protein kinase, Wnt signaling, and B- and T-cell receptor signaling in AA. A study showed that 363 genes (97 upregulated and 266 downregulated) were found to be differentially expressed in AA skin compared to nonlesional skin acting via T-cell mediated (CCL5, CXCL10, CD27, ICAM2, ICAM3, IL7R, and CX3CL1) and humoral mechanisms (IGHG3, IGHM, and CXCR5). [2]
In an experimental model natural killer (NK) cell depletion (tested by injecting anti-asialo GM1 antibodies) significantly increased perifollicular CD49b+T cells in the alopecic skin. The study shows evidence that IFN-c secreting CD49b+ T-cell subsets, by evoking strong Th1 response (cytokines IL-2, IL-12,interferon-γ and IL-1RA), are inappropriately stimulated by the receptor-activating signals released from the hair follicle epithelium and⁄or are inadequately suppressed in AA and that some NK cells are actually protective at least early on. [3]
Genetic variants in the FAS and FASLG genes (FasL or CD95L; a type-II transmembrane protein of TNF family), [4] an immune response to trichohyalin and Keratin-K16, reduced expression of red/IK cytokine (antagonist of IFNγ-induced expression of MHC class II antigens and a regulator of CD34+ cell growth) and indoleamine 2,3-dioxygenase have all been incriminated in the pathogenesis of AA. That AA shares etiology with other autoimmune disorders is suggested by establishing the involvement of the TRAF1/C5 (TNF receptor-associated factor 1, complement component 5) locus in the causation of familial and severe AA. [5]
The characteristic yellow dot pattern seen in reflectance confocal microscopy with round or polycyclic yellow-pink dots with miniaturized or broken hair shafts corresponds to the chronic phase of AA (depicting dilated infundibula of the vellus like anagen and telogen follicles). Increased serum sIL-2R level and lower IL-18 level at baseline are poor prognostic markers in AA. Coudability hairs (normal-looking hairs tapered at the proximal end) are useful in gauging the disease activity in AA and may surrogate the hair-pull test.
A variety of treatment options such as phototoxic psoralen and ultraviolet-A therapy after topical application of 0.1% 8-methoxypsoralen, diphencyprone, dinitrochlorobenzene, squaric acid dibutylester, steroids, minoxidil, anthralin, and bexarotene have shown promise in managing AA.
 References | |  |
| 1. | Nakamura M, Jo J, Tabata Y, Ishikawa O. Controlled delivery of T-box21 small interfering RNA ameliorates autoimmune alopecia (Alopecia Areata) in a C3H/HeJ mouse model. Am J Pathol 2008;172:650-8. 
[PUBMED] [FULLTEXT] |
| 2. | Subramanya RD, Coda AB, Sinha AA. Transcriptional profiling in alopecia areata defines immune and cell cycle control related genes within disease-specific signatures. Genomics 2010;96:146-53.
[PUBMED] [FULLTEXT] |
| 3. | Kaufman G, d'Ovidio R, Kaldawy A, Assy B, Ullmann Y, Etzioni A, et al. An unexpected twist in alopecia areata pathogenesis: Are NK cells protective and CD49b+ T cells pathogenic? Exp Dermatol 2010;19:347-9.
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| 4. | Fan X, Shangguan L, Li M, Li CY, Liu B. Functional polymorphisms of the FAS/FASLG genes are associated with risk of alopecia areata in a Chinese population: a case-control analysis. Br J Dermatol 2010;163:340-4.
[PUBMED] [FULLTEXT] |
| 5. | Redler S, Brockschmidt FF, Forstbauer L, Giehl KA, Herold C, Eigelshoven S, et al. The TRAF1/C5 locus confers risk for familial and severe alopecia areata. Br J Dermatol 2010;162:866-9.
[PUBMED] [FULLTEXT] |
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