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| Year : 2017 | Volume
: 60
| Issue : 2 | Page : 296-298 |
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| T helper 17 cells in atopic dermatitis: Study in a tertiary care center |
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Sharma Sudha1, Saikia Biman1, Handa Sanjeev2
1 Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
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| Date of Web Publication | 19-Jun-2017 |
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How to cite this article:
Sudha S, Biman S, Sanjeev H. T helper 17 cells in atopic dermatitis: Study in a tertiary care center. Indian J Pathol Microbiol 2017;60:296-8 |
Editor,
Atopic dermatitis (AD) is a chronic relapsing eczematous dermatitis usually seen in children before the age of 5 years and can be associated with other systemic atopic disorders.[1] Recently, the role of Th cells (T helper [TH] 17) has been suggested in its pathogenesis.[2] This study was aimed to compare absolute eosinophil count (AEC), serum IgE levels, and TH17 cell numbers in cases of AD.
Sixteen cases of AD with 16 age-matched healthy controls, seven cases of helminthic infestation (HI) with eosinophilia, and twenty adult healthy individuals-healthy controls (HC) were recruited. Cases with HI were included to see if eosinophilia and raised IgE levels are linked to raised TH17 cell numbers. Peripheral blood mononuclear cells were isolated, stimulated, and surface stained with PE-anti-CD4 antibody, followed by permeabilization and staining with Alexa Fluor-anti-IL17A and anti FITC-IFN-γ (BD Biosciences, San Jose, CA) and analyzed by flow cytometry. TH17 cells were reported as percentage of total CD4+ T cells. Serum and ethylenediaminetetraacetic acid blood was taken for serum IgE levels and AEC.
Demographic profile, AEC, serum IgE and TH17 cell numbers of cases with AD, age-matched healthy controls, HI, and HC are shown in [Table 1]. Both HI and AD had higher AEC than HC; however, HI had comparatively higher eosinophil counts. The difference in AEC in HI versus HC, AD versus HI, and AD versus HC was statistically significant (P < 0.05). Serum IgE levels were markedly raised in both AD and HI. The difference in serum IgE levels were statistically significant (P < 0.05) between HC versus AD and HC versus HI. AEC and serum IgE levels could not be performed on age-matched young healthy controls due to small amount of sample obtained in most of the children. | Table 1: Demographic profifile and results in cases of atopic dermatitis and controls
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The severity of AD was assessed based on the severity of symptoms recorded in the Outpatient Department, which was available in 11 patients. There were 3 cases with mild AD, 7 cases with moderate AD, and 1 case with severe AD. Bivariate (Pearson) correlation was used to correlate TH17 cell numbers with severity of AD, and the data showed a positive correlation (Pearson correlation = 0.644, P= 0.032).
The threshold value of normal TH17 cell numbers was determined in HC and set as >0.6% (0.6–2.84). In patients with AD, TH17 cell numbers ranged from 0.5% to 4.39%, while patients with HI had TH17 cell numbers ranging from 0.9% to 2.42%. The difference in TH17 cell numbers in AD versus HC (adults) as well as age-matched controls was statistically significant. The TH17 cell numbers in cases with HI was comparable with those of HC as well as young healthy controls. This showed that TH17 cell numbers were not affected by and did not correlate with raised IgE levels and eosinophilia that was seen in both AD and HI. Flow cytometry graph plots for TH17 cells in a patient with AD, HI, and HC are shown in [Figure 1]. | Figure 1: Flow cytometry graph plots for T helper 17 cells in a patient with atopic dermatitis, case with helminthic infestation and healthy control. The difference in T helper 17 cell numbers was statistically signifificant in HC and atopic dermatitis. T helper 17 cell numbers in HC and helminthic infestation were comparable
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AD has been considered an allergic TH2-mediated disease, characterized by abnormal IgE production, peripheral eosinophilia, mast cell activation, and induction of TH2 lymphocytes.[3] However, sequential biopsies in AD patients after exposure to aeroallergens demonstrated a biphasic immunologic response characterized by antigen presentation, TH2 activation, IgE release, eosinophil recruitment, and a switch toward TH1 phenotype in later phases of the disease.[4] A marked increase in the IL-17+CD4+ T-cell population has been previously shown in AD.[5]
Our study demonstrated that TH17 cells were increased in AD patients and also correlated with the symptom severity of AD. There was a significant difference in TH17 cell numbers in AD and HI. TH17 cell numbers were not affected by and did not correlate with raised IgE levels and eosinophilia that was seen in both AD and HC. Eczema, dermatitis (resembling AD) with eosinophilia, and raised IgE levels are also features of rare autosomal dominant hyper-IgE syndrome (HIES), and staphylococcal skin abscesses which is a feature of the latter can occur in AD due to secondary infections. TH17 cells, however, readily helps distinguish the two as TH17 cells are markedly reduced or absent in HIES but raised in AD.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
| 1. | Williams HC. Clinical practice. Atopic dermatitis. N Engl J Med 2005;352:2314-24.  [ PUBMED] |
| 2. | Di Cesare A, Di Meglio P, Nestle FO. A role for Th17 cells in the immunopathogenesis of atopic dermatitis? J Invest Dermatol 2008;128:2569-71. [ PUBMED] |
| 3. | Wierenga EA, Snoek M, Jansen HM, Bos JD, van Lier RA, Kapsenberg ML. Human atopen-specific types 1 and 2 T helper cell clones. J Immunol 1991;147:2942-9. [ PUBMED] |
| 4. | Grewe M, Walther S, Gyufko K, Czech W, Schöpf E, Krutmann J. Analysis of the cytokine pattern expressed in situ in inhalant allergen patch test reactions of atopic dermatitis patients. J Invest Dermatol 1995;105:407-10. |
| 5. | Koga C, Kabashima K, Shiraishi N, Kobayashi M, Tokura Y. Possible pathogenic role of Th17 cells for atopic dermatitis. J Invest Dermatol 2008;128:2625-30. [ PUBMED] |
Correspondence Address:
Saikia Biman
19, 4th Floor, Research Block-A, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/IJPM.IJPM_95_16
[Figure 1]
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