Assessment of Serum Interferon Gamma & Interleukin-4 inPsoriasis Vulgaris

Background: Psoriasis is T cell mediated disorder in which the cytokine network is extremely complex, involving the actions and interactions of multiple cytokines. Psoriasis vulgaris was reported to be associated with T helper cell type 1 (Th1) upregulation and T helper cell type 2 (Th2) downregulation. Objective: This cross section study was aimed to evaluate the changes in serum levels of IFN-gamma and IL4 in psoriasis vulgaris patients and correlate these parameters with psoriasis area severity index score (PASI). Subjects and methods: This work was achieved through the study of 24 psoriasis vulgaris patients (16 males, 8 females, age ranged from 24 to 62 years) and 12 age and sex matched healthy controls. They were subjected to thorough history taking, general and dermatological examination for patients and controls. PASI score was calculated for every one of psoriatic patients. IFN-gamma and IL4 serum levels were assessed for patients and control by quantitative sandwich enzyme immuneo-assay technique. The patients were classified into three groups according the duration of the disease, a group with duration up to 5 years (6 patients), a group with duration from 5 to 10 years (10 patients) and the third one with duration more than 10 years (8 patients), according to PASI score into two groups a group with PASI score up to 15 (14 patients) and a group with PASI score more than 15 (10 patients), and subdivided according to PASI score into 3 groups (group 1 with PASI score less than 13 (n=8 patients), group 2 with PASI score between 13-19 (n= 10 patients) and group 3 with PASI more than 19 (n= 6 patients). Results: The serum level of IFN-gamma was significantly higher in psoriasis vulgaris patients compared to controls and serum level of Il-4 was significantly lower in psoriasis vulgaris patients compared to controls. There was highly significant positive correlation between serum level of IFN-gamma and PASI score. There were significant inverse correlation between serum level of IL4 and each of PASI score and serum IFN-gamma. There was significant difference in the serum levels of IFN-gamma and IL4 between groups of psoriatic patients with different PASI scores, while the difference between groups with different duration of the disease was non significant. Conclusion: Psoriasis vulgaris is associated with high serum level of IFN-gamma indicating Th1 upregulation and low serum level of IL-4 indicating Th2 down regulation. These changes in IFN-gamma and IL-4 serum levels were significantly correlated to PASI score

 

Assessment of Serum Interferon Gamma & Interleukin-4 in
Psoriasis Vulgaris

Yousry M Moustafa, Ibrahim A Abdel Aal*, Mohamed Elarman*, Azza Abdel Baky* and Sahar Taher**

Departments of Dermatology & Andrology, Clinical pathology* and Medical Microbiology and Immunology**, Mansoura Faculty of Medicine, Mansoura

                                                                                                                                                                                                        

Abstract

Background: Psoriasis is T cell mediated disorder in which the cytokine network is extremely complex, involving the actions and interactions of multiple cytokines. Psoriasis vulgaris was reported to be associated with T helper cell type 1 (Th1) upregulation and T helper cell type 2 (Th2) downregulation. Objective: This cross section study was aimed to evaluate the changes in serum levels of IFN-gamma and IL4 in psoriasis vulgaris patients and correlate these parameters with psoriasis area severity index score (PASI). Subjects and methods: This work was achieved through the study of 24 psoriasis vulgaris patients (16 males, 8 females, age ranged from 24 to 62 years) and 12 age and sex matched healthy controls. They were subjected to thorough history taking, general and dermatological examination for patients and controls. PASI score was calculated for every one of psoriatic patients. IFN-gamma and IL4 serum levels were assessed for patients and control by quantitative sandwich enzyme immuneo-assay technique. The patients were classified into three groups according the duration of the disease, a group with duration up to 5 years (6 patients), a group with duration from 5 to 10 years (10 patients) and the third one with duration more than 10 years (8 patients), according to PASI score into two groups a group with PASI score up to 15 (14 patients) and a group with PASI score more than 15 (10 patients), and subdivided according to PASI score into 3 groups (group 1 with PASI score less than 13 (n=8 patients), group 2 with PASI score between 13-19 (n= 10 patients) and group 3 with PASI more than 19 (n= 6 patients). Results: The serum level of IFN-gamma was significantly higher in psoriasis vulgaris patients compared to controls and serum level of Il-4 was significantly lower in psoriasis vulgaris patients compared to controls. There was highly significant positive correlation between serum level of IFN-gamma and PASI score. There were significant inverse correlation between serum level of IL4 and each of PASI score and serum IFN-gamma. There was significant difference in the serum levels of IFN-gamma and IL4 between groups of psoriatic patients with different PASI scores, while the difference between groups with different duration of the disease was non significant. Conclusion: Psoriasis vulgaris is associated with high serum level of IFN-gamma indicating Th1 upregulation and low serum level of IL-4 indicating Th2 down regulation. These changes in IFN-gamma and IL-4 serum levels were significantly correlated to PASI score.


Introduction

Psoriasis is now regarded as T cell mediated disorder(1). CD8+ T lymphocytes seem to be dominant in the epidermis which is thought to be a key event in the pathogenesis of psoriasis, whereas the CD4+ T lymphocytes are the predominant subset in the dermis(2). The cytokine network in psoriasis is extremely complex, involving the actions and interactions of multiple cytokines, chemokines and growth factors and their receptors in addition to other mediators produced by multiple cell types(3). The psoriatic plaque is characterized by the predominance of cytokines produced by Th1 cells (IFN-gamma, IL2 and TNF-α, Th2) over those produced by th2 cells (IL4, IL5 and IL10)(4). Th1 cells cytokines (IFN-d, IL2 and TNF-α) over those produced by Th2 cells (IL4, IL-S and IL-10)(4). IFN-d is produced by NK cells, CD8 T-cells and Th1 CD8 T cells. IFNd modulates immune response, induces synthesis of multiple portions that play essential roles in antigen presentation to T cells, is required for activation of macrophages, has strong anti-proliferative effects on some cell types, is an inducer of selected chemokine, (C X C chemokine ligand 9 to 11) and is an inducer of endothelial cell adhesion molecules (e.g ICAM-1 and VCAM-1)(3). IFNd is thought to play an important role in the initiation of psoriatic lesion as demonstrate by the induction of pinpoint lesions of psoriasis at sites of IFNd injection in previously uninvolved skin(5). IL4 is a cytokine produced by activated the cells, activated NK T cells and can be released from the secretary granules of mast cells and basophils. IL-4 stimulates naïve T cells to proliferate and differentiate into Th2 cells which produce more IL-4(3). IL-4 costimulates B cells and T-cells proliferation, protects cells from spontaneous and induced apoptosis and drives immuneoglobulin class swithcing to the IgG4 IgE isotypes(6). Psoriasis is associated with relative under expression of Th2 cytokines such as IL4 and patients with genetic polymorphism of IL4 gene are susceptible to psoriasis(7).

Many studies revealed upregulated expression of IFNd and down regulated expression of IL4(7,8) in psoriasis vulgaris.

Therefore, this study was aimed to evaluate the changes is serum levels of IFNd and IL4 in psoriasis vulgaris patients and correlate them with PASI score.

Subjects and Methods

This study included 24 psoriasis vulgaris patients (16 males and 8 females) atternding the Outpatient Clinic of Dermatology Andrology Mansoura University Hospitals in the period from July 2008 to December 2008. Their ages ranged from 24 to 62 years, the mean age was 41.9 ± 12.4 years Twelve age (41.6 ± 13 years) and sex matched apparently healthy volunteers served as a control.

We excluded patients with hepatic, renal, thyroid diseases, diabetes mellitus and those receiving topical treatment apart from emollients for one month and those receiving systemic treatment or narrow band phototherapy for at least three months. All patients were subjected to carefull history taking about age, duration of psoriasis, general medical examination, as well as careful examination of the skin to assess the severity of psoriasis vulgaris by PASI score.

PASI score was calculated by summation resulting from multiplying the sum of score of four parameters of psoriasis (itching, erythema, thickness and scalling) by the score of the affected area on four body areas (head, upper limbs, trunk and lower limbs)(9). The patients were divided according the duration of the disease into three groups (group 1 from included 6 patients 2 to 5 years & group 2 from included 10 patients 6-10 years and group 3 more than 10 years duration included 8 patients). The patients were divided according to PASI score into 2 groups, group 1 with PASI score up to 15 (14 patients) and group 2 with PASI score more than 15 (10 patients). The patients were subdivided according to PASI score into 3 groups (group 1 with PASI  less than 13 included 6 patients, group 2 with PASI from 13 to 19 included 8 patients and group 3 with PASI more than 19 included 10 patients).

Six ml venous blood samples were collected from every one of patients and control subjects and divided into:

1.   One ml put on EDTA tube S for assessment of Kae and complete blood counts (sysmex 1700).

2.   Five ml put on plain tube and centrifuged for 30 minutes at 1000 RPM then serum was aliquted:

o  Routine investigations: liver functions, serum creatinine, fasting blood sugar by chemistry autoanalyzer (Cobas Integra). Another 2ml of venous blood sample was taken 2 hours after breakfast and centrifuged for estimation of post prandial blood sugar.

o  Assay of IFNd and IL4: serum was stored at - 20°C until the time of assay.

Both IFNd and IL4 were measured by quantitative sandwich enzyme immuneo-assay techenique (Quantikine T.M.R & D systems USA & Canada. WW RnD systems Com). A monoclonal antibody specific for IFNd and IL4 had been pre-coated onto microtitre plate. Standards and samples were pipette into the wells and IFNd and IL4 were bounded separately by the immobilized antibody. After washing away any unbound substances, and enzyme linked polycolonal antibody specific to the tested IFN-gamma and IL4 were added to the wells. Following a wash to remove any unbound antibody-enzyme reagent, a substrate solution was added to the wells and colour developed in proprotion to the amount of the tested IFN-gamma and IL4 which were bound in the initial step. The colour development was stopped and the intensity of the colour was measured(10).

Statistical analysis

Data were analyzed using SPSS (statistical package for social science) version 11. Qualitative variables were presented as number and percentage %). Chi-square test was used for comparison between groups. Kolomogrov-Smirov test was used to test for normaly distribution of these variables. Normally distributed variables were presented as mean ± standard deviation (SD) and student (t) test and one way ANOVA (F) tests were used for two groups and more than two groups comparison, respectively. Non parametric variables were presented as median and range and Mann-Whitney (z) and Kruskal-Wallis (KWX2) tests were used for two groups and more than two groups comparison, respectively. Spearman’s correlation coefficient was used to calculate correlation between variables. P≤ 0.05 was considered to be statistically significant.

Results

In our study the serum levels of IFN-gamma in psoriasis vulgaris patients was significantly higher (mean was 24.52) while IL4 was significantly lower (mean 4.27) than control (mean 8.33 & P= 0.004 and 12.7 P=0.000 respectively) (Table 1).

As regards the duration of psoriasis vulgaris we have found no statistical significant difference in the levels of INF-gamma (F=0.28 & P=0.76) and IL4 (F= 1.007 & P= 0.38) whatever the duration of the disease (Table 2).

Tables (3 & 4) show that there were statistical significant difference in serum levels of INF-gamma and IL-4 between the three patient groups according to PASI score (F=5.5 P=0.012 & F= 3.52 P=0.04 respectively) and when the patient were classified into two groups according to PASI score (t=3.03 P=0.006 & t=2.19 P=0.039 respectively).

There was significant correlation between PASI score and serum IFN-gamma and inverse significant correlation between both PASI score and serum IFN-gamma and serum IL-4 levels, while the correlation between the duration of psoriasis vulgaris and each of serum IFN-gamma and IL-4 was weak and non-significant (Table 5).

 

 

Table 1.    Comparison of serum levels of IFN-d and IL-4 in psoriasis vulgaris patients and control.

Parameters

Psoriasis vulgaris

Control

Significance test

 

n=24

n=12

 

IFN-gamma level

 

 

 

Mean (pg/ml)

24.52

8.33

t=3.07

SD (pg/ml)

18.09

2.27

P=0.004*

IL-4

 

 

 

Mean (pg/ml)

4.27

12.7

t=13.28

SD (pg/ml)

1.26

2.58

P=0.000*

* Significance p value.

 

Table 2.    IFN-gamma and IL4 serum levels in psoriasis vulgaris patients regarding the duration of the disease.

Parameters

2-5 years

5-10 years

> 10 years

Significance test

 

n=6

n=10

n=8

 

IFN-gamma level

 

 

 

 

Mean (pg/ml)

19.73

25.38

27.04

F=0.28

SD (pg/ml)

12.12

24.8

12.83

P=0.76

IL-4

 

 

 

 

Mean (pg/ml)

3.67

4.6

4.4

F=1.007

SD (pg/ml)

1.75

0.94

1.19

P=0.38

F One way ANOVA test

Table 3.    IFN-gamma and IL4 serum levels in psoriasis vulgaris regarding the PASI score classification into 3 groups

Parameters

PASI less than (13

PASI    (13-19)

PASI            > 19

Significance test

 

n=8

n=10

n=6

 

IFN-gamma level

 

 

 

 

Mean (pg/ml)

9.32

27.95

30.9

F=5.5

SD (pg/ml)

7.35

17.87

18.6

P=0.012*

IL-4

 

 

 

 

Mean (pg/ml)

5.5

4.00

3.74

F=3.52

SD (pg/ml)

1.01

0.73

1.29

P=0.04*

F One way ANOVA test, * significance p value.

 

Table 4.    IFN-gamma and IL-4 serum levels in psoriasis vulgaris regarding the PASI score classification into two groups

Parameters

PASI up to 15

PASI more than 15

Significance test

 

n=14

n=10

 

IFN-gamma level

 

 

 

Mean (pg/ml)

16.39

35.9

t=3.03

SD (pg/ml)

13.9

17.61

P=0.006*

IL-4

 

 

 

Mean (pg/ml)

4.71

3.65

t=2.19

SD (pg/ml)

1.27

0.99

P=0.039*

* Significance p value.

Table 4.    Correlations between IFN-gamma and IL4 serum levels and duration of the disease and PASI score in psoriasis vulgaris patients.

Parameters

Duration

of the disease

PASI score

IL4 level

IFN-gamma level

 

 

 

r

0.12

0.71

- 0.46

p

0.57

0.000*

0.005*

IL4 level

 

 

 

r

0.26

-0.42

 

p

0.21

0.039*

 

* Significance p value.

 

 

Discussion

Psoriasis vulgaris is a chronic, relapsing immune-mediated inflammatory skin disease characterized be epidermal hyperproliferation with atypical keratinocyte differentiation. T cells play the dominant role in the initiation and maintenance of psoriasis(11). Psoriasis is characterized by increased activation of T helper 1 (Th1) and down regulation of T helper 2 (Th2). Th1 produce primarily IFN-gamma and promote cell mediated immunity, whereas Th2 cells produce primarily IL4, IL5 and IL13 and promote humoral immunity. Because these cytokines and cells often counter-regulate each other, the pathogenesis of psoriasis was explained by the immune alteration in the balance between Th1 and Th2 cells rather than separate cell entities(12). IFN-gamma is believed to be an important mediator in the cytokine cascade of psoriasis(13) and is a critical element in the induction of keratinocyte hyperproliferation(14). Based on the results obtained in this study, the serum level of IFN-gamma was significantly higher in psoriasis vulgaris patients in comparison to controls (p value=0.004). This finding is consistent with the results obtained previously(15,16). The increased IFN-gamma in psoriasis vulgaris patients is produced and secreted by activated Th1 in epidermis(13,17) and mast cells(18). In our study the elevated serum level of IFN gamma was found to have significant positive correlation with PASI score and this was in agreement with Gomi et al(16). IFN-gamma serum level in our study was found to have significant negative correlation with the serum levels of IL4. This finding was in agreement with many previous studies which stated that psoriasis vulgaris was associated with upregulation of activated Th1 cells producing IFN-gamma and down regulation of Th2 cells producing IL-4(6,7,13,19,20).

IFN-gamma binding and signaling were found to be attenuated in psoriasis. The IFN-gamma receptor, the signal transducer and activator of transcription STAT-1, and the interferon regulatory factor-1 were strongly down regulated in psoriasis(21).

IFN-gamma strongly down regulated the expression of the catalytic enzymes cathepsin D and zinc-α2- glycoprotein in psoriatic skin. On the contrary it upregulates the apoptotic suppresson bcl-2. This aberrant response to IFN-gamma plays a central role in the pathophysiology of psoriasis, particularly the disruption of apoptosis and desquamation(21).

The level of IFN-gamma is over 10-fold greater in psoriatic epidermis as measured by immunohistochemistry and by polymerachain reaction(21).

In our study, we have found a significant decrease in IL4 serum level in patient with psoriasis vulgaris in comparison with controls (P=0.000). This finding was in agreement with many previous studies which stated that psoriasis vulgaris is associated with downregulation and decrease of Th2 cytokines including IL4(22,23,24). We have found a significant negative correlation between PASI score which assess the severity of psoriasis and IL4 serum level. This finding was consistent with many reports and studies which stated that improvement in psoriasis with ultraviolt B irradiation or etretinate therapy was associated with type 2 cytokine predominance with elevation of IL-4 produced by CD4+T and CD8+T cell(25) and neutrophils(26). Moreover, IL-4 therapy by subcutaneous injection was associated with more than 50% improvement in psoriasis severity in 20 patients with moderate to severe psoriasis. IL-4 therapy had shifted the immune response from Th1 to Th2(27). In another study recombinant human IL-4 therapy resulted in more than 68% improvement in PASI score in 15 out of 20 psoriatic patients New therapeutics either directed against Th1 and Th17, tumor necrosis factor, and IL12/IL23 or deviate immune responses into a protective IL4 dominated Th2 phenotype will be beneficial in psoriasis treatment protocols(29). From this study we concluded that psoriasis vulgaris is associated with high level of IFN-gamma indicating Th1 upregulation and low level of IL4 indicating Th2 downregulation. These changes in IFN-gamma and IL4 were significantly correlated to PASI score.

References

1.       Bos JD and De Rie MA (1999): The pathogenesis of psoriasis: immunological facts and speculations. Immunol Today; 20: 40-6.

2.       Koga T, Duan H, Urabek K and Furue M (2002): In situ localization of IFN-gamma positive cells in psoriatic lesional epidermis. Eur J Dermatol; 12:20-3.

3.       Williams IR, Rich BE and Kupper TS (2008): Cytokines. In Fitzpatrick's Dermatology In General Medicine. Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS and Leffell DJ 7th (eds) edition. Mc Graw Hill. New York, London, Sydney; P:1173.

4.       Valdimarsson H, Sigmundsdottir H and Jonsdottir I (1997): Is psoriasis induced by streptococcal superantigens and maintained by M-protein specific T cells that cross react with keratin? Clin Exp Immunol; 107 (suppll): 21.

5.       Fierlbeck G, Rassner G and Muller C (1990): Psoriasis induced at the injection site of recombinant interferon gamma. Arch Dermatol; 126:351.

6.       Paul WE (1991): IL-4: a proteolytic immunoregulatory lymphokine. Blood; 77: 1859-70.

7.       Kim YK, Pyo CW, Choi HB, Kim TY and Kim TG (2007): Associations of IL-2 and IL-4 gene polymorphism with psoriasis in the Korean populations. J Dermatol Sci. 48 (2): 133-9.

8.       Jiawen L, Dongsheng L and Zhijian T (2001): The expression of interleukin-17, interferon-gamma, and macrophage inflammatory protein alpha mRNA in patients with psoriasis vulgaris. J of Huazhong University of Science and Technology. Medical Sciences; 24 (3) 294-296.

9.       Jacobson CC and Kinmball AB (2004): Rethinking the psoriasis area and severity index: the impact of area should be increased. Br J Dermatol; 151 (2): 381-387.

10.     Kricka LJ, Phil D and Path FRC (2001): Principles of Immunochemical Techeniques In: Tietz Fundamentals of Clinical Chemistry. Burtis CA and Ashwood ER (eds Sth edition.WB Saunders Company. Philadelphia, London, New York, St Louis, Sydney and Toronto. P.189-190.

11.     Robert S, Sandra P, Conny HF (2007): Immunopathogenesis of psoriasis. Exp. Dermatol; 16: 779-798.

12.     David A, Randolph and Garrison FC (2006): CD4+ CD25+ regulatory T cells and their therapeutic potential. Annu. Rev. Med.; 57:381-402.

13.     Rotsztejn H, Zalewska A, Trznadel-Budzko E, Lewkowicz P, Banasik M, Tchorzewski H and Glowacka E (2005): Influence of systemic photochemotherapy on regulatory T cells and selected cytokine production in psoriatic patients: a pilot study. Med Sci Monit.; 11 (12): CR 594-8.

14.     Christophers E. (1996): The immuno pathology of psoriasis. Int Arch Allergy Immunol; 110: 199-206.

15.     Chodorowska G (1998): Plasma concentrations of IFN-gamma and TNF-α in psoriatic patients before and after local treatment with dithranol ointment. J Eur Acad Dermatol Venereol; 10: 147-151.

16.     Gomi T, Shiohara T, Mumaka T, Imanishi I and Nagashima M (1991): Interleukin 1α, tumor necrosis α, and interferon gamma in psoriasis. Arch Dermatol; 127: 827-830.

17.     Szabo SK, Hammerberg C, Yoshida Y, Bato-Csorgo 2 and Cooper KD (1998): Identification and quantification of interferon-gamma producing T vells in psoriatic lesions localization to both CD4+ and CD8+ subsets. J Invest Dermatol; 111 (6): 1072-1078.

18.     Ackermann L, Harvima IT, Pelkonen J, Ritamaki-Salo VRJ and Horsmanheimon (1999): Mast cells in psoriatic skin are strongly positive for interferon-gamma. Br. J. Dermatol; 140 (4): 624-633.

19.     Van den Oord JJ, De ley M and Peeters C (1995): Distribution of interferon-gamma receptors in normal and psoriatic skin. Pathology, Research and Practice; 191 (6): 530-4.

20.     Szabo-SK, Hammerberg C, Yoshida Y, Bata-Csorgo Z and Cooper KD (1998): Identification and quantification of interferon-gamma producing T cells in psoriatic lesions: localization to both CD4+ and CD8+ subsets. J Invest Dermatol; 111 (6): 1072-8.

21.     Chen SH, Arany I, Apisarnthanarax N, Rajaraman S, Tyring SK, Horikoshi T, Brysk H and Brysk MM (): Response of keratinocytes from normal and psoriatic epidermis to interferon-gamma differs in the expression of zinc-α2 glycoprotein and cathepsin-D.

22.     Ovigne JM, Baker BS, Brown DW, Powles AV and Fry L (2001): Epidermal CD8+ T cells in chronic plaque psoriasis are. Experimental Dermatology; 10 (3): 168-174.

23.     Jain S, Kaur IR, Das S, Bhattacharya SN and singh A. (2009): T helper 1 to T helper 2 shift in cytokine expression: an autoregulatory process in superantigen associated psoriasis progression? J Med Microbiol.; 58 (pt2): 180-4.

24.     Buske-kirschbaum A, Kern S, Ebrecht M, Hellhammer DH (2007): Altered distribution of leukocyte subsets production in response to acute psychological stress in patients with psoriasis vulgaris. Brain Behav Immun.; 21 (1): 92-9.

25.     Kano Y, Teraki Y and Shiohara T. (2006): Dramatic improvement of psoriatic erythroderma after acute hepatitis: analysis of cytokine synthesis capability in peripheral blood T cells. Br J Dermatol; 155 (2): 455-9.

26.     Piskin G, Tursen U, Bos JD and Teunissen MBM. (2003): IL-4 expression by neutrophils in psoriasis lesional skin upon high dose UVB exposure. Dermatology; 207 (1) 51-53.

27.     Komarroff AL (2003): Interleukin-4 therapy improves psoriasis. Nat Med.; 9: 40-6.

28.     Bradbury J (2002): Immune deviation with IL-4 could prove beneficial in psoriasis. The Lancet; 360 (9348): 1845.

29.     Ghoreschi K, Weigert C and Rocken M (2007): Immunopathogenesis and role of T cells in psoriasis. Clin Dermatol; 25 (6): 574-80.

 

 

 

تقييم مستوي الجاما إنترفيرون والانترلوكين-4 في مرضي الصدفية الشائعه

يسري محمد مصطفي - ابراهيم أحمد عبد العال*  -محمد العرمان* - عزه عبد الباقي* - سحر طاهر**

من اقسام الجلدية والتناسلية وطب الذكوره والباثولوجيا الاكلينيكية* والميكروبيولوجيا والمناعه الطبيه**بكلية الطب- جامعة المنصورة

تعتبر الصدفية مرض ناتج عن خلل في عمل الخلايا تي والتي تحتوي علي شبكه معقده من السيتوكينات شامله عمل وتفاعل عدد من السيتوكينات. وقد دون ان الصدفيه الشائعه يصاحبها نشاط في الخلايا المساعده تي 1 وتثبيط في الخلايا المساعده تي 2.

وقد تم عمل هذا البحث لتقييم التغيرات في مستويات الجاما انترفيرون والانترليكوين 4 في مرضي الصدفيه الشائعه وكشف علاقه هذه البيانات مع مقياس شدة الصدفيه (باسي).

وتم عمل هذا البحث علي اربع وعشرين مريضا بالصدفية الشائعه (16 ذكر و8 اناث تتراوح اعمارهم بين 24 و62 عاما) واثنتي عشره من الاصحاء متماثلين في العمر والجنس كمجموعه ضابطة. وتم اخذ تاريخ مرضي وعمل فحص عام وجلدي للمرضي والمجموعه الضابطه. وتم حساب مقياس شدة الصدفيه (باسي) لكل واحد من مرضي الصدفيه وتم قياس مستوي الجاما انترفيرون والانترليوكين 4 للمرضي والمجموعه الضابطه بطريقه القياس المناعي الانزيمي الكمي.

وتم تقسييم المرضي الي ثلاثة مجموعات تبعاً لزمن المرض وتبعاً لمقياس شدة المرض (باسي) الي مجموعتين مجموعه ذات مقياس باسي الي 15 (14 مريضاً) ومجموعه ذات مقياس باسي اكثر من 15 (عشرة مرضي) وتم تقسييم المرضي مره اخري تبعاً لمقياس شدة المرض باسي الي ثلاثة مجموعات ومجموعه 1 بمقياس باسي اقل من 13 (8 مرضي) ومجموعه 2 بمقياس باسي من 13 الي 19 (عشرة مرضي) ومجموعه 3 بمقياس باسي اكثر من 19 (6 مرضي).

وقد وجدت زيادة ذات دلاله احصائيه في مستوي الجاما انترفيرون ونقص ذو دلاله احصائية في مستوي الانترليوكين 4 في المصل في مرضي الصدفيه الشائعه عن المجموعه الضابطه وقد وجدت علاقة موجبه ذات دلاله احصائية بين مستوي الجاما انترفيرون في المصل ومقياس شدة المرض (باسي). ووجد علاقة عكسية ذات دلالة احصائية بين مستوي الانترليوكين-4 في المصل وكل من مقياس باسي ومستوي الجاما انترفيرون في المصل. وقد وجد اختلاف ذو دلالة احصائية في مستوي الجاما انترفيرون والانترليوكين4 في المصل بين مجموعات مرضي الصدفيه ذات المقياس باسي المختلف بينما كان الاختلاف بين المجموعات المقسمه تبعاً لزمن المرض ليس له دلاله احصائية.

ومن هذا البحث نستنتج ان الصدفيه الشائعه تكون مصاحبه بزيادة في مستوي الجاما انترفيرون في المصل مشيراً الي زيادة نشاط الخلايا المساعده تي 1 ونقص في مستوي الانترليوكين4 مشيراً الي نقص في نشاط الخلايا المساعده تي 2. وهذه التغيرات في مستوي الجاما انترفيرون والانترليكوين4 في المصل ذات علاقة وطيده مع مقياس شدة المرض (باسي).

 

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