Serum Interleukin 17 and Interleukin 33 in Vitiligo Egyptian Patients

Rapid Communication

Austin J Dermatolog. 2021; 8(1): 1093.

Serum Interleukin 17 and Interleukin 33 in Vitiligo Egyptian Patients

Ibrahim ElGhareeb M*, Elmokadem S, Fathi M, Khalifa N and Gado M

Department of Dermatology, Zagazig University, Egypt

*Corresponding author: Mohamed Ibrahim ElGhareeb, Department of Dermatology, Zagazig University, Egypt

Received: December 15, 2020; Accepted: January 07, 2021; Published: January 14, 2021

Abstract

Background: Vitiligo is an acquired depigmented disorder characterized by milky-white macules in the skin. Interleukin-17 has important role in autoimmune diseases development like vitiligo. Interleukin-33 is released after tissue damage or cell death. It may reflect recent disease activity.

Aim: To measure serum levels of IL17 and IL-33 in vitiligo patients and to assess their relationship with disease activity.

Methods: Levels of IL17 and IL-33 in serum samples taken from 21 healthy normal subjects and 21 vitiligo patients were measured by ELISA. All the patients were subjected to careful history taking , general examination and local examination to assess extent ,activity of vitiligo and VASI score.

Results: IL17 and IL-33 serum levels were highly statistically significant increase in patients with vitiligo than the normal control subjects(p≤0.001). Their levels were related to disease activity and the extent of the disease. Interleukin 17 serum levels were positively correlated with IL-33 serum levels.

Conclusion: Increased serum levels of IL-17 and IL-33 in vitiligo patients and their levels were related to disease activity and the extent of the disease indicating that IL-17 and IL-33 may play a role in the pathogenesis of vitiligo.

Introduction

Vitiligo pathogenesis was explained by many theories like autoimmune, neurogenic, genetic, autocytotoxic, microenvironmental hypotheses [1]. The role of autoimmunity in vitiligo is supported by the presence of autoantibodies against melanocytes, and presence of perilesional T-lymphocytes infiltrates [2].

Cytotoxic CD8+ T lymphocytes are the responsible cells of melanocytes destruction. Many cytokines secreted within the skin help those T cells to be directed to targeted melanocytes. Interferons increases the expression of CXCL10, which allows tissue invasion by cytotoxicT-cells. It has been reported increased expression of other cytokines as IL-17 and IL-33 in patients with vitiligo [3].

IL-17 binds to its receptor on keratinocytes, which leads to increase in the production of IL-1β, IL-8, IL-6, and TNF-a that may lead to melanocyte destruction. IL-17 effects on keratinocytes also include the upregulation of human β -defensin 2 and CCL20 gene expression [4]. CCL20 together with VEGFs increase the migration of cytotoxic T cells as well as neutrophils to the targeted melanocytes. Neutrophils migration leads to increase in ROS production. ROS may destroy melanocytes directly or indirectly through increased production of IL-1,IL-6, and TNF-a from the surrounding keratinocytes that eventually lead to melanocytes destruction [5,6].

IL-33 increases Th1 cytokines, as IFN- γ. Cytotoxic T cells expresses IL-33 receptor which is called ST2L on their cell surface [7].

It was found that IL-33 levels were increased in both blood and tissue samples in vitiligo patients. The expression of ST2 receptors in tissue samples were also increased [8].

IL-33 affects the function of keratinocytes that surround the targeted melanocytes by inhibiting the release of SCF and bFGF (which are paracrine melanogenic factors) , and at the same time increasing TNF- a and IL-6 release(which are paracrine melanocyte destroying factors). Peripheral nerve endings in the vitiliginous skin microenvironment release neuropeptides, as corticotropin- releasing hormone and neurotensin that synergize with IL-33 [9,10].

Methods

Twenty one vitiligo patients (14 females and 7 males) were enrolled in the study with age ranging from 8 to 65 years. Twenty one age-matched healthy subjects (13 females and 8 males) were used as controls. The duration of vitiligo ranged from 1 to 42 years.

None of the patients had immune mediated comorbidities such as insulin-dependent diabetes, atopic dermatitis or psoriasis. Patients had to refrain from systemic therapy for vitiligo for at least 4 weeks before the study. All the patients were subjected to careful history taking, general examination and local examination to assess extent, activity of vitiligo and VASI score. Nine patients (42.9%) had segmental vitiligo while 12 patients (57.1%) had non-segmental vitiligo. Eight patients (38.1 %) were stable while 13 patients (61.9%) had active vitiligo. The VASI ranged from 2.5%- 14.25% ,with mean of 6.71±3.67. Family history of vitiligo was present in 8 vitligo patients.

Upon informed consent, a blood sample(6ml), performed for routine analysis, was taken to determine the circulating serum levels of IL-17 and IL-33. Serum levels of IL-17 and IL-33 were measured in the patients and controls using sandwich Enzyme-Linked Immunosorbent Assay (ELISA) kit according to the manufacturer’s recommendations. Data were expressed as ng/L.

The collected data were analyzed by computer using Statistical Package of Social Services version 24 (SPSS).

Results

IL - 17 and IL-33 serum levels were highly statistically significant increased in vitiligo patients as compared with controls (p≤0.001) (Table 1).