Biphasic Cytokine Expression by T Cell Clones From Patients With Atopic Dermatitis With Different Incubation Periods and Strengths of Stimuli

Kanek, R; Matsu, T; Iwatsuki, Keiji; Motok, Y; Oyama,; Kaneko, Fumio

doi:10.5387/fms.47.51

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…Our group has previously experienced varying results in IL‐5 analyses with low levels in AKC patients in an eyelid treatment study , but more often, IL‐5 has been reported as typically elevated in AKC patients , and an increase at 8 and possibly 48 h after provocation could have been expected parallel to an influx of eosinophils . Possibly, repeated challenge or an even higher allergen dose could have induced more pronounced changes , but in a previous study in SAC patients, we found a single high‐dose provocation suitable for a sufficient response and this was here proven safe also for AKC patients.…”

Section: Discussionmentioning

confidence: 96%

Conjunctival provocation with airborne allergen in patients with atopic keratoconjunctivitis

Nivenius

Ploeg

Gafvelin

et al. 2011

Clin Experimental Allergy

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Section: Discussionmentioning

confidence: 96%

Conjunctival provocation with airborne allergen in patients with atopic keratoconjunctivitis

Nivenius

Ploeg

Gafvelin

et al. 2011

Clin Experimental Allergy

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“…Lymphocytes that infiltrate to AD lesional skin in the initial phase of the disease are Th2‐type cells that produce Th2 cytokines 1 , such as interleukin (IL)‐4 and IL‐5. Even in chronic stages of the disease, under Th1‐type conditions, interferon (IFN)‐γ production 2 may occur with or without IL‐4. The pathomechanisms for these processes are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Effects of ultraviolet-inactivated herpes simplex virus type I on atopic dermatitis-like lesions in NC/Nga mice: Role of the suppressor of cytokine signaling in the skin

Horiuchi

Bae

Katayama

et al. 2004

Allergology International

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Background: Atopic dermatitis (AD) is characterized by repetitious eczematous skin and is Th2 dominant in nature. Atopic dermatitis lesions have been observed to improve in patients during viral or bacterial infection, such as herpes simplex virus (HSV). A Th1 pathway established to counter viral infection may possibly be the mechanism for the relief of skin lesions in AD. Methods: In animal AD models using NC/Nga mice, the effects of local intra‐ and/or subcutaneous injection of ultraviolet inactivated‐HSV were examined for Th1/Th2 regulation through a negative regulation pathway with suppressor of cytokine signaling (SOCS)‐3 and 5 using immunohistochemistry, in situ hybridization and reverse transcription−polymerase chain reaction. Results: Lesional skin of HSV‐treated mice displayed extensive interleukin (IL)‐12p40‐positive cellular infiltration compared with non‐treated mice and IL‐12p40/signal transducers and activators of transcription (STAT) 4/SOCS5 mRNA expression was noted basically the same in the three groups. Interleukin‐4 receptor‐positive cellular infiltrates in HSV‐treated mice decreased significantly more than in non‐treated mice and IL‐4 mRNA expression in the three groups was essentially the same, but the expression of STAT6 and SOCS3 mRNA specific for the Th2 regulation pathway was reduced more in HSV‐treated compared with non‐treated mice. Expression of SOCS3 mRNA in situ in HSV‐treated epidermis underwent a far greater reduction compared with expression in non‐treated mice. Conclusions: Ultraviolet‐inactivated HSV treatment would appear to induce a Th1 cellular response and downregulate that of the Th2 pathway in AD‐like lesions of NC/Nga mice by bringing about a reduction of SOCS3 expression in the skin. From the present results, certain HSV DNA components may be effective candidates for a new therapeutic approach in refractory AD.

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“…In AD-lesions, the production of TSLP, a critical activator of Th2 inflammation 39 , as well as Th2-related cytokines such as IL-4, IL-5, and IL-13 can enhance AD progression 40 . Furthermore, the production of cytokines such as CC17 41 , IFN-γ 42 and IL-17 43 adds to the development of AD. We measured the expression of these cytokines in the AD-lesion by quantitative real-time PCR (Figure 3 G).…”

Section: Resultsmentioning

confidence: 99%

IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells

Yue,

Hu,

et al. 2024

Int. J. Biol. Sci.

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Atopic dermatitis (AD) is a common inflammation skin disease that involves dysregulated interplay between immune cells and keratinocytes. , a poorly characterized IL-1 family cytokine, its role and mechanism in the pathogenesis of AD is elusive. Here, we show that IL-38 is mainly secreted by epidermal keratinocytes and highly expressed in the skin and downregulated in AD lesions. We generated IL-38 keratinocyte-specific knockout mice (K14 Cre/+ -IL-38 f/f ) and induced AD models by 2,4-dinitrofluorobenzene (DNFB). Unexpectedly, after treatment with DNFB, K14 Cre/+ -IL-38 f/f mice were less susceptible to cutaneous inflammation of AD. Moreover, keratinocyte-specific deletion of IL-38 suppressed the migration of Langerhans cells (LCs) into lymph nodes which results in disturbed differentiation of CD4 + T cells and decreased the infiltration of immune cells into AD lesions. LCs are a type of dendritic cell that reside specifically in the epidermis and regulate immune responses. We developed LC-like cells in vitro from mouse bone marrow (BM) and treated with recombined IL-38. The results show that IL-38 depended on IL-36R, activated the phosphorylated expression of IRAK4 and NF-κB P65 and upregulated the expression of CCR7 to promoting the migration of LCs, nevertheless, the upregulation disappeared with the addition of IL-36 receptor antagonist (IL-36RA), IRAK4 or NF-κB P65 inhibitor. Furthermore, after treatment with IRAK4 inhibitors, the experimental AD phenotypes were alleviated and so IRAK4 is considered a promising target for the treatment of inflammatory diseases. Overall, our findings indicated a potential pathway that IL-38 depends on IL-36R, leading to LCs migration to promote AD by upregulating CCR7 via IRAK4/NF-κB and implied the prevention and treatment of AD, supporting potential clinical utilization of IRAK4 inhibitors in AD treatment.

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Biphasic Cytokine Expression by T Cell Clones From Patients With Atopic Dermatitis With Different Incubation Periods and Strengths of Stimuli

Cited by 4 publications

References 22 publications

Conjunctival provocation with airborne allergen in patients with atopic keratoconjunctivitis

Conjunctival provocation with airborne allergen in patients with atopic keratoconjunctivitis

Effects of ultraviolet-inactivated herpes simplex virus type I on atopic dermatitis-like lesions in NC/Nga mice: Role of the suppressor of cytokine signaling in the skin

IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells

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