Suppressive Effects of Mesenchymal Stem Cells in Adipose Tissue on Allergic Contact Dermatitis

BACKGROUND: Allergic contact dermatitis (ACD), which is accelerated by interferon (IFN)-γ and suppressed by interleukin (IL)-10 as regulators, is generally self-limited after removal of the contact allergen. Adipose tissue-derived multipotent mesenchymal stem cells (ASCs) potentially exert immunomodulatory effects. Considering that subcutaneous adipose tissue is located close to the site of ACD and includes mesenchymal stem cells (MSCs), the MSCs in adipose tissue could contribute to the self-limiting course of ACD. OBJECTIVE: The aims of the present study were to elucidate the effects of MSCs in adipose tissue on ACD and to examine any cytokine-mediated mechanisms involved. METHODS: Ear thickness in a C57BL/6 mouse model of ACD using contact hypersensitivity (CHS) elicited by 2,4,6-trinitro-1-chlorobenzene was evaluated as a marker of inflammation level. Five and nine mice were injected with ASCs and phosphate-buffered saline (PBS), respectively. After ASC or PBS injection, real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed. RESULTS: Histology showed that CHS was self-limited and ear thickness was suppressed by ASCs in a dose-dependent manner. IFN-γ expression in the elicited skin site and regional lymph nodes was significantly lower in ASC-treated mice than in control mice. IL-10 expression did not differ between treated and control mice. The suppressive effects of ASCs on CHS response did not differ between IL-10 knock-out C57BL/6 mice and wild-type mice. CONCLUSION: The present findings suggest that MSCs in adipose tissue may contribute to the self-limiting course of ACD through decreased expression of IFN-γ, but not through increased expression of IL-10.

Chronic Toxoplasmosis Modulates the Induction of Contact Hypersensitivity by TNCB in Mouse Model

Mouse models of chronic toxoplasmosis and atopic dermatitis (AD) were combined to clarify the effect of opportunistic Toxoplasma gondii infection on the development of AD. AD was induced as a chronic contact hypersensitivity (CHS) with repeated challenge of 2,4,6-trinitro-1-chlorobenzene (TNCB) on the dorsal skin of mice. TNCB induced skin thickness increases in both normal and toxoplasmic mice. The changing patterns were different from the sigmoidal which saturated at 20 days in normal mice to the convex saturated at 12 days in toxoplasmic mice with the crossing at 18 days. Compared to normal mice, toxoplasmic mice presented CHS more severely in earlier times and then moderately in later times. These data suggest that host immune modification by T. gondii infection enhances CHS in early times of atopic stimulation but soothes the reaction of CHS in later times in mouse model.

Role of mast cell in the late phase of contact hypersensitivity induced by trimellitic anhydride / 대한해부학회지

Mast cells are known as effector cells of IgE-mediated allergic responses, but role of mast cells in contact hypersensitivity (CHS) has been considered controversial. In this study, we investigated role of mast cell in trimellitic anhydride (TMA)-induced CHS. The mice were sensitized to TMA on the back and repeatedly challenged with TMA on the left ear at 1-week intervals. The ear after challenge showed biphasic responses. The repetition of TMA challenge shifted in time course of ear response and enlarged the extent of early and late phase reactions in proportion to the frequency of TMA challenges in C57BL/6 mice. In late phase reaction, peak of ear response by single challenge showed at 24 hours after challenge, but the peak by repeat challenges at 8 hours after the last challenge. Number of mast cells and eosinophils per unit area increased in proportion to frequency of TMA challenges. However, mast cell-deficient WBB6F1/J-Kit(W)/Kit(W-v) mice developed the late phase reaction without the early phase reaction. The repetition of TMA challenge shifted in time course of ear response and enlarged the extent of ear response and the infiltration of eosinophils. The magnitude of these responses observed according to the frequency of the TMA challenge in mast cell-deficient WBB6F1/J-Kit(W)/Kit(W-v) mice was significantly lower than that in C57BL/6 mice. Also TMA elicited mast cell degranulation and histamine release from rat peritoneal mast cells in a concentration-dependent manner. Conclusively, TMA induces the early and late phase reactions in CHS, and mast cells may be required for TMA-induced CHS.

Pharmacodynamic analysis and related mechanisms of pseudolaric acid B on contact hypersensitivity / 中国药理学通报

Aim To investigate the pharmacodynamic experiment and molecular mechanisms of a diterpenoid from cortex pseudolaricis, pseudolaric acid B ( PB ) , on immunoregulation. Methods The mouse models of contact hypersensitivity ( CHS) were induced by 2,4-dinitrofluorobenzene ( DNFB ) . Then , the ear swelling and spleen index were measured after administered o-rally with PB. The pathological changes such as in-flammatory cell infiltration in ear skin were observed by hematoxylin and eosin ( HE ) staining. Besides, the expression of peroxisome proliferater-activated receptorγ ( PPARγ) and the phosphorylation of Akt were ana-lyzed by Western blot. The activity of PPARγ was fur-ther detected by luciferase reporter gene assay. Results The results showed that PB could both alleviate the ear thickness, inhibit the spleen index, and reduce the inflammatory degree of their ear skin, which might be involved in inducing PPARγexpression and activation, associated with suppressing Akt signaling pathway. Conclusion It is suggested that PB might regulate PPARγ-related Akt pathway, which indicates the pos-sibility of developing PB as a novel immunoregulation agent for treating inflammatory-immune disease.

The Effect of Topical Tacrolimus in the Murine Contact Hypersensitivity and Dermatitis of Repeated Applications Induced by Diphenylcyclopropenone / 대한피부과학회지

BACKGROUND: Topical tacrolimus is widely used for the treatment of inflammatory skin diseases like atopic dermatitis, but there are few studies about the effect of topical tacrolimus for allergic contact dermatitis. Allergic contact dermatitis develops in two phases, the clinically silent sensitization phase, and the clinically apparent elicitation phase. OBJECTIVE: The purpose of this study is to investigate whether topical tacrolimus has an effect on both phases of murine contact hypersensitivity and dermatitis of repeated applications induced by diphenylcyclopropenone (DPCP). METHODS: Hairless mice were treated with topical tacrolimus before and after DPCP challenging. The suppressive effect of topical tacrolimus was measured by skin erythema, ear swelling, weight change and cell numbers of local lymph nodes. In addition, a biopsy was carried out and epidermal hyperplasia was investigated microscopically. TNF-alpha mRNA on the mice which were treated with topical tacrolimus to one side of the ears was measured before and after being chronically challenged with DPCP on both ears. RESULTS: Topical tacrolimus pretreatment dramatically supressed inflammatory reactions in the sensitization phase, and treatment of topical tacrolimus after sensitization dramatically supressed inflammatory reactions in the elicitation phase. Topical tacrolimus also dramatically supressed inflammatory reactions in the repeated DPCP-induced dermatitis. CONCLUSION: The data revealed topical tacrolimus could effectively suppress murine contact hypersensitivity and dermatitis of repeated applications induced by DPCP. Putting these results together, topical tacrolimus can be very effective in not only the treatment but also the prevention of allergic contact dermatitis. Larger studies are needed to determine the clinical relevance.

Effects of the Photostability of Sunscreens on the in vivo Photoprotection / 대한피부과학회지

BACKGROUND: Solar ultraviolet (UV) radiation induces sunburn, immune suppression, and various pigmentary disorders. Sunscreens are widely used to protect those untoward effects by UV but there are reports of phototoxicity or stability problems of sunscreens after exposure to UV. OBJECTIVE: We tried to compare sunscreens with different photostability in terms of their protection against various biologic responses like sunburn, immune suppression or pigmentation. METHODS: Three different sunscreens with SPF around 30 were used; Sunscreen-A (Sc-A) was photochemically inert, sunscreen-B (Sc-B) showed intermediate level of photostability, and sunscreen-C (Sc-C) was the least stable. To observe their in vivo effects, we measured sunscreen-protection against sunburn by back-skin swelling and sunburn cell formation, against immune suppression measured by depletion of Langerhans cells, local and systemic suppression of contact hypersensitivity (CHS), and against pigmentation by irradiation with mixed light source with UVA and UVB lamps that mimic solar UV spectrum. RESULTS: Back skin swellings by 5 kJ/m2 of UVB were protected well by sunscreens, but protection of Sc-C against 50 kJ/m2 of UVB was worse than Sc-A or Sc-B. Sunburn cells were increased significantly in mice irradiated with 5 kJ/m2 of UVB and it was protected by sunscreens, and the effect of photostability was minimal. Depletion of epidermal Langerhans cells by 5 kJ/m2 of UVB was protected completely by sunscreens. Local suppression of CHS by 5 kJ/m2 of UVB was protected by sunscreens, and Sc-A had better protection. But, in the experiment with 50 kJ/m2 of UVB, the protective efficacy was reversed; Sc-A showed worse protection. Systemic suppression of CHS by 10 kJ/m2 of UVB was protected well by sunscreens, and Sc-A had better protection and Sc-C had worse protection. In the experiment irradiated with 100 kJ/m2 of UVB, the protection of sunscreens was decreased, and Sc-B showed better protection, whereas Sc-C showed worse protection. In UV-induced pigmentation, all three sunscreens showed significant protection both by L* value and individual topographic angle (ITA) with the best protection by Sc-A and the worst protection by Sc-B. CONCLUSION: These data showed sunscreens can protect various in vivo responses and photostability of sunscreens played important roles particularly in the back-skin swelling and systemic suppression of CHS by high dose of UVB.

Glucosides of Chaenomeles speciosa suppressed contact hypersensitivity response via modulating the thymus T lymphocytes subsets in mice / 中国药理学通报

Aim To investigate the effects and mechanisms of glucosides of chaenomeles speciosa (GCS) in mice with contact hypersensitivity (CHS) response. Methods CHS model in mice induced by 2,4-dinitro-I-dinitroflurobenzene (DNFB) was used in this study. Concanavalin A (Con A)-induced splenocytes proliferation was measured by the MTT colorimetric method and interleukin-2 (IL-2) activity was measured by testing its ability to support ConA-induced mice splenocytes proliferation by MTT method. Interleukin-4 (IL-4) and transforming growth factor -beta 1 (TGF-? 1) levels were determined by ELISA. T lymphocytes subsets were measured by flow cytometry. Results Similar as the control drug 4-acetylaminophenylacetic acid (actarit or Acta) (120 mg?kg -1), GCS (240 mg?kg -1) could inhibit the thymus index and spleen index in CHS mice. GCS( 60,120,240 mg?kg -1) could inhibit the ear swelling of CHS mice and could inhibit the splenocytes proliferation induced by ConA. GCS (240 mg?kg -1)decreased CD4 +CD8 +T lymphocytes subsets ratio and resumed the CD4 +CD8 -subsets ratio in CHS mice;GCS(240,60 mg?kg -1) resumed the CD4 -CD8 -subsets ratio in CHS mice. GCS also decreased the TGF-? 1 and IL-2 levels and increased the IL-4 levels in mice thymus with CHS. Conclusion GCS could inhibit mice CHS reaction and resume the balance of T lymphocytes subsets in mice thymus with CHS, and also could modulate the cytokines production by CD4 + T lymphocytes of CHS mice.

A Murine Model of Toluene Diisocyanate-induced Contact Hypersensitivity

BACKGROUND: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/J-Kit(W)/ Kit(W-v) (W/W(V)) and congenic normal WBB6F1/J-Kit +/+ (+/+) mice. METHODS: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, W/W(V) and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of W/W(V) and +/+ mice at 24 hours after 1% TDI challenge. RESULTS: TDI induced a significant ear swelling response in W/W(V) and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in W/W(V) and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus W/W(V) mice, either at baseline or after TDI-induced CHS. CONCLUSION: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.

A Murine Model of Toluene Diisocyanate-induced Contact Hypersensitivity

BACKGROUND: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/J-Kit(W)/ Kit(W-v) (W/W(V)) and congenic normal WBB6F1/J-Kit +/+ (+/+) mice. METHODS: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, W/W(V) and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of W/W(V) and +/+ mice at 24 hours after 1% TDI challenge. RESULTS: TDI induced a significant ear swelling response in W/W(V) and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in W/W(V) and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus W/W(V) mice, either at baseline or after TDI-induced CHS. CONCLUSION: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.

Immunologic Mechanism of Experimental and Therapeutic Ultraviolet B Responses

The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.

The Effect of High Dose UVA - 1 and UVA - 2 Irradiation on the Expression of Surface Markers of Epidermal Langerhans Cells and Induction of contact Hypersensitivity in Mice Skin / 대한피부과학회지

BACKGROUND: It is knovn that Langerhans cells are damaged fuctionally and morphologically by UV irradiation. Recently, high-dose UVA-1 therapy (340-400nm) was introduced as an effective treatment of severe exacerbated atopic dermatitis. However, the effect of UVA-1 therapy on surface markers and function of epidermal Langerhans cells are still unclear. OBJECTIVE: To determine whether a high dose UVA-1 irradiation affects cutaneous immune system, the effect of UVA-1 on the expression of ATPase and Ia antigen of mouse epidermal Langerhans cells and induction of contact hypersensitivity in mice skin were investigated and were compared to those of UVA-2. METHODS: Balb/c mice were irradiated with 150J/cm and 300J/cm of UVA-1 and UVA-2 in a single dose at one time or 3 fractionated doses for 3 days. The number of Langerhans cells was evaluated using ATPase and immunoperoxidase-stained epidermal sheets. Balb/c mice were irradiated with same manner after induction of contact hypersensiyity by applying 0.5% oxazolone solution and the influence of UV irradiation was evaluated by measuring the ear swelling of mice. RESULTS: 1. The expression of surface markers of Langerhans cells was not affected by 150J/cm and fractionated 300J/cm of UVA-1. However, single irradiation of 300J/cm of UVA-1 reduced signifi-cantly the expression of surface markers. The irradiation of UVA-2 induced more prominent reduction of the expression of surface markers compared to UVA-l. 2. Although the induction of contact hypersensitity was not inhibited in groups irradiated by single or fractionated 150J/cm of UVA-1, it was inhibited in groups irradiated with 300J/cm of UVA-1. The inhibition of contact hypersensitivity induction by UVA-2 irradiation was also more prominent than that by UVA-1. CONCLUSION: These results suggest that epidermal Langerhans cells could be damaged by high doses of UVA-1 and the damage of Langerhans cells by UVA-1 is weaker than that by UVA-2.

High Doses of UVA Suppress Contact Hypersensitivity

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.

High Doses of UVA Suppress Contact Hypersensitivity

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.

Hyperthermia Depletes Epidermal Langerhans Cells and Modulates Contact Hypersensitivity Reaction in Mice

This study was designed to investigate the effect of local hyperthermia on contact hypersensitivity (CHS) and elucidate it's mechanism through assessment of number of epidermal LCs and transfer of spleen cells. Depilated dorsal skin of mouse was immersed into controlled water bath at 52 ℃ for 30 seconds in vivo. The number of epidermal LCs was counted by adenosine triphosphate staining, and CHS to 2,4-dinitro-l-fluorobenzene was assessed by ear swelling and transfer of spleen cells. The number of LCs was significantly reduced 1 to 3 days after the hyperthermia treatment and recovered to normal 5 days after the treatment. CHS was significantly suppressed in mice sensitized 5,7, or 10 days after hyperthermia treatment, but the suppression was meager in mice sensitized 1 or 3 days after the treatment. There is a discord between the number of LCs and degree of CHS. When mice received spleen cells from hyporesponsive donors, CHS was remarkably sup-pressed in the recipient mice compared with positive control. These findings suggest that tfeatment of local hyperthermia suppress CHS in mice, which may be associated with the induction of suppressor cells. The nature of the discord between the the number of LCs and degree of CHS in this investigation remains to be cleared by further studies.

Inhibition of Contact Hypersensitivity by PUVA Treatment

Normal C3WHeN strain mice exposed to topical 8inethoxypsomlen plus long wave ultraviolet (PUVA) showed a reduction in contact hypersensitivity, (CH) which was localized to the skin in the area of PUVA treatment (local suppression), whereas systemic PUVA treatment caused diffuse suppression of CH reaction, regardless of the application site of 2,4-dinitro-1-fluorobenzene (DNFB). There seem to be two different mechanisms responsible for CH reduction by PUVA. Local suppression by topical PUVA treatment was thought to be a result of blocking the afferent phase of immune response, it was associated with a lack of CH effector cells in the peripheral lymph nodes and could not be reversed by indomethacin treatment. Diffuse suppression induced by systemic PUVA treatment seemed to be associated with blocking of egress of effector cells from the regional lymph nodes, this depressed CH response was prevented when indomethacin was administered before PUVA treatment.

Elucidation of the Inhibitory Immune Mechanism of the Contact Hypersensitivity in Mice Induced by Ultraviolet Irradiation / 대한피부과학회지

Normal C3H/HeN strain mice exposed to low-dose ultraviolet radiation(4 * 400 J/m) demonstrated a reduction in contact sensitization potential which locaiized to the skin area of direct UVR exposure(local suppression), where high-dose exposure of UVR(1*30.000 J/m) caused systemic suppression of CH induction, regardless of the application site of 2,4-dinitro-l-fluorobenzene(DNFB). There seemed to be two different mechanisms that are responsible for CH reaction induced by UVR. One of them, local suppression of low-dose UVR resulted from blocking the afferent phase of immune response by the functiona] inactivation of the epidermal Langerhans cells ; it was associated with lack of CH effector cells in the peripheral lymph nodes, an enhanced splenic suppressor cell acitvity, and could not be reversed by indomethacin treatment. The other, systemic suppression of high-dose UVR was mediated by enhancement of prostaglandin E(PGE); it was associated with prevention of the egress of effector cells within the regional lymph node which was caused by blocking the efferent lymphatics, and elevated plasma level of PGE. And depressed CH response was reversed when treated by indomethacin.

Time course of contact hypersensitivity to DNFB and histologic findings in mice

This experiment pursued the time course of contact hypersensitivity to 2,4-dinitro-1-fluorobenzene (DNFB) and histologic changes of the cutaneous reaction in mice. The contact hypersensitivity reached a maximum 4 days after sensitization (96.9 +/- 6.7% vs. 22.7 +/- 1.3% in control) and persisted for 3 weeks. The cutaneous hypersensitivity reaction showed peak reactivity at 24 hr after challenge (96.2 +/- 4.7% vs. 11.5 +/- 1.7% in control), and persisted up to 96 hr (13.2 +/- 2.1%). Prime histologic changes observed in this experiment were the exocytosis of lymphoid cells and epidermal thickening which appeared at 20 hr after challenge. Edema, vasodilatation and increased mast cells were observed within the dermis at 4-8 hr. However, edema and vasodilatation disappeared gradually, but numbers of mast cell increased up to 96 hr. The dermal infiltrates were maximum at the 28-72 hr after challenge.

Cyclosporin Modulates DNCB Contact Hypersensitivity Reaction in Guinea Pigs / 대한피부과학회지

CsA per os during the early sensitization period caused potentiation of 14-day shin response and this response was enhanced in group D, CsA given on days 3 7 Thereafter, suppression of CHS began in group E, CsA was given on days 6- 1G, and this tendency continue to the time of full sensitization of guinea pigs (group G). 27701173 We report herein a case of alopecia mucinosa in a 46-year-old male. He had a coin-sized erythematous hairless plaque on the parietal area. Histopathologic examinations, including much stains, showed typical findings of alopecia mucinosa. Thc present case, appeared on the scalp, might be an acute benign type of the disease.